2trivia Flashcards

1
Q

parietal lobe

A

Damage to the right side of
the parietal lobe can result in difficulty navigating spaces,
even familiar ones. If the left side is injured, the ability to
understand spoken and/or written language may be impaired.

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2
Q

spinal cord length

A

about 17 inches (43

cm) long

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3
Q

axon length

A

range in length from a tiny fraction of an inch (or centimeter)
to three feet (about one meter) or more

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4
Q

neuron number

A

The
mammalian brain contains between 100 million and 100
billion neurons, depending on the species.

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5
Q

glia number

A

The brain contains at least ten times more glia than

neurons.

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6
Q

ACh

A

acetylcholine, the first neurotransmitter to be identified, about 80 years ago

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7
Q

myasthenia gravis cause

A

Antibodies that block one
type of ACh receptor cause myasthenia gravis. The immune system attacks the junctions where
nerves connect with muscles

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8
Q

ACh and dementia

A

Because
ACh-releasing neurons die in Alzheimer’s patients, finding
ways to restore this neurotransmitter is a goal of current
research. Drugs that inhibit acetylcholinesterase — and
increase ACh in the brain — are presently the main drugs
used to treat Alzheimer’s disease.

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9
Q

GABA (and disease)

A

The activity of GABA is increased by
benzodiazepines (e.g., valium) and by anticonvulsant drugs.
In Huntington’s disease, a hereditary disorder that begins
during midlife, the GABA-producing neurons in brain
centers that coordinate movement degenerate, causing
uncontrollable movements.

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10
Q

NMDA receptor stimulation

A

The stimulation of NMDA receptors may promote
beneficial changes in the brain, whereas overstimulation can
cause nerve cell damage or cell death. This is what happens
as a result of trauma and during a stroke.

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11
Q

NMDA and medicine

A

Developing
drugs that block or stimulate activity at NMDA receptors
holds promise for improving brain function and treating
neurological and psychiatric disorders.

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12
Q

catecholamines

A

The term catecholamines includes

the neurotransmitters dopamine and norepinephrine.

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13
Q

dopamine is present in __ principal circuits in the brain:

A

3;
movement – Parkinson’s
cognition and emotion – schizophrenia
regulation of endocrine system

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14
Q

dopamine and Parkinson’s

A

The dopamine
circuit that regulates movement has been directly linked
to disease. Due to dopamine deficits in the brain, people
with Parkinson’s disease show such symptoms as muscle
tremors, rigidity, and difficulty in moving. Administration of
levodopa, a substance from which dopamine is synthesized,
is an effective treatment for Parkinson’s, allowing patients to
walk and perform skilled movements more successfully

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15
Q

dopamine and mental illness

A

Another dopamine circuit is thought to be important for
cognition and emotion; abnormalities in this system have been
implicated in schizophrenia. Because drugs that block certain
dopamine receptors in the brain are helpful in diminishing
psychotic symptoms, learning more about dopamine is
important to understanding mental illness.

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16
Q

dopamine and the endocrine system

A

In a third circuit,
dopamine regulates the endocrine system. Dopamine directs
the hypothalamus to manufacture hormones and hold them in
the pituitary gland for release into the bloodstream or to trigger
the release of hormones held within cells in the pituitary.

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17
Q

Korsakoff’s syndrome

A

a cognitive disorder associated with chronic

alcoholism. patients have deficiencies in norepinephrine

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18
Q

norpenephrine and disease

A

Deficiencies in norepinephrine occur in patients with
Alzheimer’s disease, Parkinson’s disease, and Korsakoff’s
syndrome. These conditions all lead to memory loss and a
decline in cognitive functioning. Thus, researchers believe
that norepinephrine may play a role in both learning and
memory.

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19
Q

norpinephrine release

A

Norepinephrine is also secreted by the sympathetic
nervous system throughout the body to regulate heart
rate and blood pressure. Acute stress increases release of
norepinephrine from sympathetic nerves and the adrenal
medulla, the innermost part of the adrenal gland.

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20
Q

serotonin and medicine

A

Because serotonin controls different
switches affecting various emotional states, scientists believe
these switches can be manipulated by analogs, chemicals
with molecular structures similar to that of serotonin. Drugs
that alter serotonin’s action, such as fluoxetine, relieve
symptoms of depression and obsessive-compulsive disorder.

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21
Q

substance P

A

Some sensory
nerves — tiny unmyelinated C fibers — contain a peptide
called substance P, which causes the sensation of burning
pain. The active component of chili peppers, capsaicin,
causes the release of substance P, something people should be
aware of before eating them

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22
Q

discovery of opioid peptides

A

In
1973, scientists discovered receptors for opiates on neurons
in several regions of the brain, suggesting that the brain must
make substances very similar to opium. Shortly thereafter,
scientists made their first discovery of an opiate peptide
produced by the brain. This chemical resembles morphine,
an opium derivative used medically to kill pain. Scientists
named this substance enkephalin, literally meaning “in
the head.” Soon after, other types of opioid peptides
were discovered. These were named endorphins, meaning
“endogenous morphine.”

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23
Q

FSH and LH in females

A

In females, these hormones act on
the ovary to stimulate ovulation and promote release of
the ovarian hormones estradiol and progesterone.

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24
Q

FSH and LH in males

A

In males,
these hormones are carried to receptors on cells in the testes,
where they promote spermatogenesis and release the male
hormone testosterone, an androgen, into the bloodstream.

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25
aspirin
Aspirin reduces a fever and lowers pain | by inhibiting the cyclooxygenase enzyme.
26
second messenger effects
Second messenger effects may endure for a few milliseconds to as long as many minutes. They also may be responsible for long-term changes in the nervous system.
27
The intricate communication systems in the brain and | the nervous system begin to develop __
about three weeks after | gestation.
28
H.M.
A major breakthrough in understanding how the brain accomplishes learning and memory began with the study of a person known by his initials, H.M. As a child, H.M. developed a severe, difficult-to-treat form of epilepsy. When traditional therapies didn’t help, H.M. underwent an experimental surgical treatment — the removal of the medial regions of his temporal lobes. The surgery worked in that it greatly alleviated the seizures, but it left H.M. with severe amnesia. He could remember recent events for only a few minutes and was unable to form explicit memories of new experiences. For example, after talking with him for a while and then leaving the room, upon returning, it would be clear that H.M. had no recollection of the exchange. Despite his inability to remember new information, H.M. remembered his childhood very well.
29
what did researchers learn from H.M.?
researchers concluded that the parts of H.M.’s medial temporal lobe that were removed, including the hippocampus and parahippocampal region, played critical roles in converting short-term memories of experiences to long-term, permanent ones. Because H.M. retained some memories of events that occurred long before his surgery, it appeared that the medial temporal region was not the site of permanent storage but instead played a role in the organization and permanent storage of memories elsewhere in the brain.
30
ASD
Autism spectrum disorders (ASD) are characterized by impaired social skills; verbal and nonverbal communication difficulties; and narrow, obsessive interests or repetitive behaviors.
31
ASD rate
One of every 110 babies born in the United States, approximately 40,000 new cases each year, is diagnosed with ASD, an incidence far greater than in the 1970s.
32
there is currently no single genetic or biochemical biomarker specifically for autism, because no single gene mutation or biological change will predict the disorder. Therefore, at this time, there is no way to determine if a newborn child is at risk for autism
read
33
ADHD numbers
Attention deficit hyperactivity disorder (ADHD) was first described more than 100 years ago. ADHD affects an estimated 5 to 8 percent of school-age children. Studies show that as many as 60 percent of these children will continue to experience ADHD symptoms as adults.
34
ADHD symptoms
Symptoms of ADHD appear by middle childhood, last for six months or longer, and impair normal functioning to a significant degree
35
ADHD treatment
ADHD is commonly treated with parent education, school-based interventions, and medications such as stimulants (e.g., methylphenidate) and newer, nonstimulant drugs.
36
ADHD and the brain
Increasingly, studies are finding correlations between ADHD and differences in brain function. Altered activity is often observed in circuits connecting the cortex, the striatum, and the cerebellum, particularly in the right hemisphere. Recent studies show a delay in cortical development in some children with ADHD, although most individuals with ADHD do not outgrow the disorder as they mature.
37
ADHD and maturation
most individuals with ADHD do not outgrow the disorder as they mature. Rather, their symptoms often change as they grow older, with less hyperactivity as adults. Problems with attention tend to continue into adulthood.
38
ADHD and genes
Twin and family studies show that ADHD has a strong genetic influence, and genes encoding components of dopamine and norepinephrine transmission have been implicated. Recent imaging studies have shown reduced catecholamine transmission in at least some patients with this disorder. Because prefrontal circuits require an optimal level of catecholamine stimulation, reduced catecholamine transmission could lead to weakened prefrontal cortical regulation of attention and behavior and symptoms of ADHD.
39
prenatal diagnoses of Down syndrome
Prenatal screening tests, such as the triple and quadruple screen blood tests, can accurately detect Down syndrome in about 70 percent of fetuses. Definitive prenatal diagnoses can be obtained with either chorionic villus sampling or amniocentesis.
40
genetic basis of Down syndrome
It typically occurs when, at the time of conception, an extra copy of chromosome 21 — or part of its long arm — is present in the egg or, less commonly, in the sperm. It is not known why this error occurs, and it has not been linked to any environmental or behavioral factors, either before or during pregnancy
41
Down syndrome rate
Down syndrome, the most frequently occurring chromosomal condition, appears in 1 of every 691 babies, or about 6,000 babies annually in the United States.
42
Down syndrome and moms
At age 25, the risk is about 1 in 1,250 births; at age 40, it is 1 in 100. Because of higher fertility rates in younger women, 80 percent of children with Down syndrome are born to women under 35 years of age.
43
Down syndrome is associated with approximately __ | physical and developmental characteristics.
50
44
Down syndrome: physical characteristics
low muscle tone; an upward slant to the eyes; a flat facial profile; an enlarged tongue
45
Down syndrome: health characteristics
increased risk of congenital heart | defects, respiratory problems, and digestive tract obstruction.
46
Down syndrome and aging
By age 40, nearly all people with Down syndrome show some neurological changes similar to those seen in Alzheimer’s disease, and most show cognitive decline by age 60.
47
An estimated __ of children in the United States have some form of learning disability involving difficulties in the acquisition and use of listening, speaking, reading, writing, reasoning, or mathematical abilities.
8 - 10 percent
48
dyslexia rate
Dyslexia, a specific reading disability, is the most common and most carefully studied of the learning disabilities. It affects 80 percent of all those identified as learning disabled, or as many as 15 to 20 percent of Americans.
49
There is now a strong consensus that the central | difficulty in most forms of dyslexia reflects
a deficit within the language system — more specifically, in a component of the language system called phonology
50
dyslexia and brain imaging
Converging evidence derived from functional brain imaging indicates that dyslexic readers demonstrate a functional inefficiency in an extensive neural system in the posterior portion of the brain. The brain images that result from these studies are referred to as the neural signature of dyslexia.
51
dyslexia and brain regions
A range of investigations indicates that there are differences in brain regions between dyslexic and nonimpaired readers involving three important left hemisphere neural systems, two posteriorly (parietotemporal, occipito-temporal) and one anteriorly around the left inferior frontal region (Broca’s area).
52
dyslexia and genetics
It is clear that dyslexia runs in families, but initial hopes that dyslexia would be explained by one or just a few genes have not been realized. Current evidence suggests that dyslexia is best conceptualized within a multifactorial model, with multiple genetic and environmental risk and protective factors leading to dyslexia.
53
GWAS
Genome-wide association studies (GWAS) in dyslexia have so far identified genetic variants that account for only a very small percentage of the risk — less than 1 percent — making it unlikely that a single gene or even a few genes will identify people with dyslexia.
54
dyslexia treatment
Interventions to help children with dyslexia focus on teaching the child that words can be segmented into smaller units of sound and that these sounds are linked with specific letter patterns. In addition, children with dyslexia require practice in reading stories.
55
drug abuse rate, cost
Drug abuse is one of the nation’s most serious health problems. About 9 percent of Americans, more than 22 million people, abuse drugs on a regular basis. Drug abuse, including alcohol and nicotine, is estimated to cost the United States more than $600 billion each year.
56
nicotine numbers, cost, [most]
In 2009, more than 70 million Americans smoked. In fact, tobacco kills more than 440,000 U.S. citizens each year. Tobacco use is the leading preventable cause of death in the United States. The overall cost of smoking in the United States is estimated to be $193 billion each year.
57
newer treatments for nicotine adidction
bupropion, varenicline
58
bupropion
The first non-nicotine prescription drug, bupropion, an antidepressant, has been approved for use as a pharmacological treatment for nicotine addiction.
59
varenicline
An exciting advance is the use of varenicline for smoking cessation. This medication interacts directly with the acetylcholine nicotinic receptor in a key part of the brain’s reward circuitry and prevents nicotine from activating this circuit.
60
alcohol and the liver
Cirrhosis, or scarring of the liver, is the main chronic health problem associated with alcohol addiction. Other chronic liver diseases are responsible for more than 29,000 deaths each year.
61
alcohol and genetics
It is clear that genetic and environmental factors contribute to alcoholism, but at this point, no single factor or combination of factors enables doctors to predict who will develop an addiction to alcohol.
62
alcohol numbers, cost, [most]
Nearly17.6 million people abuse alcohol or are alcoholic. Fetal alcohol syndrome, affecting about 1 to 3 of every 1,000 babies born in the United States, is the leading preventable cause of mental retardation. The annual cost of alcohol abuse and addiction is estimated at $185 billion.
63
alcohol medication
Earlier, a medication called naltrexone had been developed for heroin addiction, which also affects the opioid system. Naltrexone works by blocking opioid receptors. Researchers thought that this medication might be effective for alcoholics as well.
64
naltrexone use
Clinical trials began in 1983, and in 1995, the U.S. Food and Drug Administration (FDA) approved naltrexone for the treatment of alcoholism.
65
endocannabinoids and medication
Scientists recently discovered that cannabinoid receptors normally bind to natural internal chemicals termed endocannabinoids, one of which is called anandamide. A large effort is now being made to develop medications that target the endogenous, or internal, cannabinoid system. The hope is that these medications will prove beneficial in treating a number of different brain disorders, including addiction, anxiety, and depression.
66
opiate addiction medication number
Buprenorphine has been prescribed for more than 500,000 patients in the United States.
67
psychostimulant use numbers
In 2009, in the United States, an estimated 4.8 million | people age 12 and older had abused cocaine.
68
date-rape drugs
Rohypnol, GHB, and ketamine are predominantly | central nervous system depressants. often colorless, tasteless, odorless; added easily to drinks
69
Alzheimer's rate
Rare before age 60 but increasingly prevalent in each decade thereafter, Alzheimer’s affects 5 percent of Americans age 65 to 74 and nearly half of those age 85 and older. As many as 5.3 million Americans have Alzheimer’s.
70
Alzheimer's prediction
The disease is predicted to affect approximately 14 million | individuals in the United States by the year 2050.
71
Alzheimer's rank
seventh leading cause of death in the United States and the fifth leading cause of death for Americans aged 65 and older
72
Alzheimer's and genetics
Early-onset Alzheimer’s disease is a rare, dominantly inherited form of the disease. Recently, scientists have identified Alzheimer’s disease-associated mutations. The gene encoding the amyloid precursor protein (APP) is on chromosome 21. In some families with early-onset Alzheimer’s, mutations have been identified in the presenilin 1 and 2 genes.
73
Alzheimer's medication
Five drugs have been approved by the FDA to treat Alzheimer’s. Four prevent the breakdown of acetylcholine, a brain chemical important for memory and thinking. (nerves cells utilising the chemical transmitter acetylcholine are particularly vulnerable to attack in Alzheimer's) The fifth regulates glutamate, a brain chemical that may cause brain cell death when produced in large amounts.
74
future Alzheimer's medication
Several | other approaches, such as antioxidants, are being tested.
75
ALS cost
The costs of both care and treatment for ALS are expensive, and they continue to rise as the disease progresses. In the final stages, ALS can cost as much as $200,000 a year per family, and costs Americans some $300 million annually.
76
ALS number
This progressive disorder strikes approximately 5,600 Americans annually, with an average survival time of just two to five years from symptom onset. It is the most common disorder within a group of diseases affecting motor neurons. Typically, 30,000 Americans have the disease at any given time.
77
ALS medication
An anti-glutamate drug slows | the disease’s progression modestly.
78
ALS and genetics
Scientists have now identified several genes that are responsible for some forms of ALS. The most common and well-studied of these are mutations in the gene that codes for superoxide dismutase, a defense against oxidative distress.
79
ALS detection
No specific test identifies ALS, but electrical tests of muscle activity, muscle biopsies, blood studies, computed tomography (CT), and magnetic resonance imaging (MRI) scans help diagnose the disease and rule out other disorders.
80
ALS causes
- >90 percent of the time, it's sporadic; Potential causes or contributors to the disease include an excess amount of the neurotransmitter glutamate, which becomes toxic; oxygen in a dangerous form in the body, resulting in what is called oxidative distress; environmental factors; and an autoimmune response in which the body’s defenses turn against body tissue. - In the other 5 to 10 percent of cases, ALS is familial — transmitted to family members because of a gene defect.
81
first signs of ALS
usually seen in the hands and feet or in the muscles of speech and swallowing
82
ALS death
usually caused by | respiratory failure or pneumonia.
83
Huntington's numbers
Affecting some 30,000 Americans and placing 200,000 more Americans at risk for inheriting the disease from an affected parent, Huntington’s disease is now considered one of the most common hereditary brain disorders.
84
Huntington's progression
progresses slowly over 10 - 20 yr period and appears btwn the ages of 30 and 50
85
Huntington's symptoms
The most recognizable symptoms include involuntary jerking movements of the limbs, torso, and facial muscles. These are often accompanied by mood swings, depression, irritability, slurred speech, and clumsiness. As the disease progresses, common symptoms include difficulty swallowing, unsteady gait, loss of balance, impaired reasoning, and memory problems.
86
Huntington's and genetics
gene that causes it was identified in 1993. The Huntington’s disease mutation is an expanded triplet repeat — a kind of molecular stutter in the DNA. This abnormal gene codes for an abnormal version of the protein called huntingtin. The huntingtin protein, whose normal function is still unknown, is widely distributed in the brain and appears to be associated with proteins involved in transcription (turning genes on), protein turnover, and energy production. Scientists suspect that Huntington’s disease is caused by the gain of a new and toxic function among these proteins
87
Parkinson's causes
Typically, people start showing symptoms over the age of 50. In fact, aging is the only known risk factor for the development of this disorder. Although the cause of Parkinson’s remains unknown, most researchers believe that there are both genetic and environmental factors that contribute to the injury and eventual loss of these dopamine-producing cells. While most cases of Parkinson’s do not appear to be inherited, there are certain situations in which genetic factors may be involved.
88
Parkinson's numbers
Parkinson’s disease is a progressive neurological disorder that affects approximately 1.5 million individuals in the United States.
89
Parkinson's on a cellular level
Parkinson’s disease is the result of the loss of dopamine-producing cells in the region of the brain called the substantia nigra pars compacta, found in the midbrain. A large number, 40 percent, of cells must be lost before symptoms occur, suggesting that perhaps the brain has a way of warding off symptoms. Eventually, however, these mechanisms begin to fail, or the continued loss of cells leads to a threshold from which the brain can no longer recover.
90
Parkinson's symptoms/effects/characteristics
Parkinson’s disease is characterized by slowness of movement, muscular rigidity, and walking and balance impairment. Many affected individuals may develop a resting tremor as well. Besides impairment in motor movement, Parkinson’s may also cause changes in non-motor brain function.
91
Parkinson's medication
The discovery in the late 1950s that the level of dopamine was decreased in the brains of Parkinson’s patients was followed in the 1960s by successful treatment with the drug levodopa, which is converted to dopamine in the brain. This historical event is one of the greatest medical breakthroughs in the field of neurology. a drug called carbidopa is often combined with levodopa; the combination is effective in that it reduces the breakdown of levodopa in the bloodstream, allowing greater levels of dopamine to reach the brain. It also reduces side effects, such as nausea.
92
Parkinson's medication weaknesses
dopamine replacement therapy neither cures the disease nor slows its progression. In addition, dopamine replacement is not optimal for treating non-motor aspects of the disease, such as anxiety and sleep issues. What’s more, this treatment becomes less effective over time in helping with gait and balance problems.
93
Huntingont's and brain regions
It affects both the basal ganglia, which controls coordination, and the brain cortex, which serves as the center for thought, perception, and memory.
94
MPTP
One common rodent and nonhuman primate model uses the neurotoxin MPTP, first discovered in the late 1970s, when it was accidentally synthesized by designers of illicit drugs looking for ways to produce a heroin-like compound. The drug addicts who self-injected the MPTPcontaminated preparations developed a neurological condition that was indistinguishable from Parkinson’s. Researchers soon found that MPTP is converted in the brain to a substance that destroys dopamine neurons. This finding led to using MPTP as a tool for medical studies.
95
future Parkinson's treatments
- surgically implanting cells, such as fetal cells, that are capable of producing dopamine - replacement therapy w/ stem cells is being explored - gene transfer of trophic factors is in clinical trials - gene therapy in clinical trials
96
current newer Parkinson's treatments
- past decade has witnessed a resurgence in pallidotomy - More recently, chronic deep-brain stimulation has been used. These techniques are highly successful for treating patients who have experienced significant worsening of symptoms and are troubled by the development of drug-related involuntary movements.
97
anxiety disorders numbers
Considered the most common mental illnesses, anxiety disorders affect an estimated 18 percent of the adult population in a given year, or 40 million Americans.
98
OCD medication
- the serotonergic antidepressant clomipramine, which was the first effective treatment developed for people with OCD - other serotonergic antidepressants, as well as selective serotonin reuptake inhibitors (SSRIs) such as sertraline and paroxetine, are effective in treating OCD.
99
other OCD treatment
A specialized type of behavioral intervention, called exposure and response prevention, also is effective in many patients
100
OCD in animals
Scientists have recently discovered that certain breeds of large dogs develop acral lick syndrome, severely sore paws from compulsive licking. These dogs respond well to clomipramine
101
OCD and brain imaging
Positron emission tomography (PET) scans reveal abnormalities in both cortical and deep areas of the brain, implicating central nervous system changes in individuals with OCD.
102
OCD causes
Neuroscientists think that environmental factors and | genetics probably play a role in the development of the disorder.
103
OCD and maturation
One-third of | adults develop their symptoms as children.
104
OCD number
The illness is estimated to | affect 2.2 million American adults annually.
105
panic disorder rate
a lifetime | prevalence rate of 4.7 percent in the United States
106
panic disorder treatment
Antidepressants, including SSRIs, are effective, as | is cognitive behavioral therapy.
107
phobia treatment
Cognitive behavioral therapy | is an effective treatment.
108
phobias on a cellular level
It is likely that panic disorders and phobias have similar neurochemical underpinnings that emerge as the result of a particular “stressor.”
109
panic disorders on a cellular level
It is likely that panic disorders and phobias have similar neurochemical underpinnings that emerge as the result of a particular “stressor.”
110
PTSD rate
lifetime prevalence rate of 6.8 percent (9.7 percent in women and 1.8 percent in men)
111
PTSD medication
The alpha-1 blocker prazosin, a drug used to lower blood pressure for more than 20 years, is now used to treat nightmares experienced with PTSD. People treated with prazosin include those with a very long-standing illness, such as Holocaust survivors. Beta-blockers such as propranolol also are being tested in individuals exposed to trauma, but these agents must be administered shortly after the trauma, before PTSD has been established, which brings up complex ethical issues. PTSD also is treated with antidepressant and atypical antipsychotic medications
112
other PTSD treatment
PTSD also is treated with antidepressant and atypical antipsychotic psychotherapies, such as cognitive behavioral therapy or eye movement desensitization and reprocessing therapy.
113
PTSD on a cellular level
Scientists have studied PTSD in depth and have learned that the very high levels of norepinephrine released in the brain during stress remain at heightened levels. Medications that work well for patients with PTSD have emerged from basic research into norepinephrine’s actions in different brain regions.
114
endogenous antianxiety
The discovery of brain receptors for the benzodiazepine antianxiety drugs has sparked research to identify the brain’s own antianxiety chemical messengers. Benzodiazepines bind to GABA receptors and enhance responsiveness to endogenous GABA, the major inhibitory neurotransmitter in the brain. Indeed, recent studies have revealed alterations in certain GABA receptors in the central nervous system of patients with PTSD, effectively providing an additional neurochemical link between different anxiety disorders. This finding may lead to new ways to modulate anxiety disorders.
115
Tourette and genetics
One of the most common and least understood neurobiological disorders, Tourette syndrome is an inherited disorder that affects about 200,000 Americans. Males are affected three to four times as often as females.
116
Tourette numbers
The symptoms include motor and vocal tics — repetitive, involuntary movements or utterances that are rapid, sudden and persist for more than one year. The types of tics may change frequently and increase or decrease in severity over time.
117
Tourette complications
A high percentage of people with Tourette syndrome also have associated conditions, such as problems with learning, difficulties with attention, obsessive thoughts and compulsive rituals. Often these manifestations are more troublesome to individuals than the tics themselves, so physicians must consider them when choosing a treatment regimen.
118
Tourette and maturation
In roughly one-half of individuals, this disorder lasts a lifetime, but the remaining patients may experience a remission or decrease in symptoms as they get older. Symptoms usually appear between the ages of four and eight, but in rare cases may emerge in the late teenage years.
119
Tourette non medication treatment
Behavioral therapies, such as those used to treat similar disorders that emerge in childhood, have been receiving more attention. Aimed at training circuits to control the specific behavior related to the tic, these therapies have proven to be highly effective in reducing the severity of tics in some subtypes of Tourette syndrome. Psychotherapy and counseling can assist people with this disorder, as well as providing coping mechanisms for family members.
120
Tourette medication
The majority of people with Tourette syndrome are not significantly disabled by symptoms, so they do not require medication. However, antipsychotics and SSRIs, as well as drugs to control tics, nausea, high blood pressure, seizures, or anxiety, are available to help control symptoms when they interfere with functioning. Stimulant medications such as methylphenidate and dextroamphetamine, which are prescribed for attention deficit hyperactivity disorder (ADHD), have been reported to improve attention and decrease tics in Tourette syndrome.
121
depressed individuals' response to treatment
80 percent of these individuals respond to drugs, psychotherapy, or a combination of the two. Some severely depressed patients can be helped with electroconvulsive therapy / deep brain stimulation approaches (originally developed for patients w/ neurodegenerative disease)
122
date rape drug and depression
Recently, ketamine, a drug that blocks NMDA glutamate receptors, has been shown to alleviate depressed symptoms rapidly. Because ketamine has many side effects, it is not likely to be used clinically, but these findings have set off an exciting search for new pharmacologic approaches.
123
bipolar disorder rate
Bipolar disorder that is characterized by full manic episodes and depressions affects about 1 percent of the population worldwide. When people who suffer from hypomania along with depressions are factored in, the prevalence goes up to 2.6 percent. This finding is based on a study of Americans over the age of 18. In addition, about the same number of men and women suffer from bipolar disorder.
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bipolar disorder and genetics
Bipolar disorder is highly influenced by genes. In fact, many different genes contribute to the risk of the disorder. Modern technology has allowed us to identify a small number of these genes. The study of the genetic basis of bipolar disorder continues to be a very active area of research.
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bipolar disorder medication
lithium. During the late 1940s, researchers showed that when guinea pigs were injected with lithium, they became placid, implying that the lithium had a mood-stabilizing effect. When given to manic patients, lithium improved all manic symptoms and stabilized their moods. + depression treatments
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schizophrenia cost
Annual costs total about $62.7 billion.
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schizophrenia numbers
about 1.1 percent of the population, or | 2.4 million Americans
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schizophrenia medication: 1st gen
The first generation of antipsychotic drugs acts by inhibiting certain dopamine receptors. This mechanism accounts for the high prevalence of side effects, similar to those seen with Parkinson’s, that are associated with the use of firstgeneration antipsychotics. The mechanism also explains the risk of developing an irreversible movement disorder, tardive dyskinesia, which results in aimless, uncontrollable movements, such as grimacing or rapid eye blinking
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1st antipsychotic drug
The first antipsychotic drug, chlorpromazine, was discovered by accident in the 1950s and shown to reduce symptoms of schizophrenia. Clinical trials demonstrated that chlorpromazine was more effective than a placebo or a sedative. Subsequently, more than 20 effective antipsychotic drugs were developed.
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schizophrenia medication: 2nd gen
The second generation of antipsychotic medications were developed to be more effective in treating the positive symptoms of schizophrenia. They do not have the same likelihood of causing Parkinsonian effects but can lead to other debilitating side effects, such as very large weight gain, blood disorders, and muscle pain and dysfunction.
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schizophrenia and genetics
Schizophrenia leads to changes that may be caused by the disruption of neurodevelopment through a genetic predisposition, which may be exacerbated by environmental factors such as maternal infections or direct brain trauma. Recently, mutations in several genes involved in controlling nerve cell communication have been identified that appear to increase the risk of developing schizophrenia.
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schizophrenia and brain imaging
Functional neuroimaging scans such as PET and functional magnetic resonance imaging (fMRI) taken while individuals perform cognitive tasks, particularly those involving memory and attention, show abnormal functioning in specific brain areas of people with this illness.Brain scans and postmortem studies show abnormalities in some people with schizophrenia, such as enlarged ventricles (fluid-filled spaces) and reduced size of certain brain regions.
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schizophrenia and brain systems
Brain systems using the chemicals dopamine, glutamate, and GABA appear to be particularly involved in the development of the disorder.
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brain tumor number and rate
The incidence of primary brain tumors is about 19 cases per population of 100,000. About 35,000 new cases occur in the United States annually.
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brain tumor symptoms
Symptoms of brain tumors vary according to the tumor’s location and size, but seizures and headaches are among the most common. An expanding tumor can increase pressure within the skull, causing headache, vomiting, visual disturbances, and impaired mental functioning.
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brain tumor imaging
Brain tumors are diagnosed | with MRI and CT scanning.
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brain tumors and neurotransmitters
gliomas, typically malignant brain tumors, release the neurotransmitter glutamate at toxic concentrations. The glutamate kills off neurons near the tumor, making room for its expansion. The released glutamate is largely responsible for the seizures, which originate from tissue surrounding the tumor
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brain tumor treatments
Surgery is generally the first step if the tumor is accessible and vital structures will not be disturbed. Radiation is used to stop a tumor’s growth or cause it to shrink. Chemotherapy destroys tumor cells that may remain after surgery and radiation, but it is not very effective for gliomas, largely because it is hard for chemotherapeutic drugs to reach the brain.
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brain tumor meds
Steroid drugs relieve brain swelling and antiepileptic | drugs control seizures.
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MS numbers
Multiple sclerosis (MS) is a lifelong ailment of unknown origin that affects approximately 400,000 Americans and 2.5 million people worldwide.
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MS diagnosis age
MS is diagnosed mainly in | individuals between the ages of 20 and 40.
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MS cost
In fact, in the United States, the disease results in earnings losses of about $10.6 billion annually for individuals with MS and their families.
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MS and genetics
Siblings of people with MS are at a 2 to 3 percent risk of developing MS (10 to 15 times higher than the general population), whereas the risk for an identical twin of someone with MS is much higher — about 30 percent. Caucasians are more susceptible than other races.
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MS and the environment
the disease is as much as five times more prevalent in temperate zones, such as the northern United States and northern Europe, than it is in the tropics. Previous studies had suggested that those who developed MS before the age of 15 were affected by environmental factors, but more recent, larger studies suggest that there is no exact age cutoff.
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types of MS
Symptoms due to an acute attack may last from several weeks to months and then spontaneously improve. This form of MS is known as relapsing/remitting. If, however, there is ongoing nerve fiber degeneration, symptoms become permanent and gradually worsen, causing progressive MS. This form of MS leads to a progressive accumulation of disability usually affecting mobility, strength, balance, and coordination. At this point, MS cannot be cured.
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MS meds
several medications help control relapsing/remitting forms of MS by lixmiting the immune attack and reducing associated inflammation. mattacks can be made shorter using drugs such as steroids that dampen down the immune system. For patients with severe MS, some doctors believe that permanently dampening down certain parts of the immune system with drugs like azathioprine or ß-interferon can be beneficial.
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HAND rate
HIV-associated neurocognitive disorder (HAND) is a common complication affecting more than 50 percent of people with HIV. Milder forms of HAND have been reported in 30 to 40 percent of HIV-infected people who are medically asymptomatic.
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HAND problems
Individuals with HAND have mental problems ranging from mild difficulty with concentration, memory, complex decision-making or coordination to progressive, fatal dementia. advanced disease: leg weakness and loss of balance
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HAND and brain imaging
Imaging techniques, such as CT and MRI, show that the brains of these patients have undergone some shrinkage. Examination of the brains of persons dying with AIDS can reveal loss of neurons, abnormalities in the white matter (tissue that serves to connect different brain regions), and injury to cellular structures that are involved in signaling between neurons. There also may be inflammation and vessel disease.
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HAND hypothesis
Despite advances in treating other aspects of the disease, HAND remains incompletely understood. Most current hypotheses center on an indirect effect of HIV infection related to secreted viral products or cell-coded signal molecules called cytokines.
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HIV products and HAND
Some proteins of the virus itself are neurotoxic and may play a role in the ongoing damage that occurs during infection. Viral Tat, released by infected cells, has been among the proteins suspected of neurotoxicity.
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HAND meds
Recent studies indicate that highly active combination antiretroviral treatment (CART)— cocktails of three or more drugs active against HIV — is effective in reducing the incidence of severe HAND, termed AIDS dementia. Such treatment also can reverse, but not eliminate, the cognitive abnormalities attributed to brain HIV infection.
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HIV neuropathy effects
Peripheral neuropathy, a type of nerve injury in extremities that causes discomfort ranging from tingling and burning to severe pain
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neuropathy rate
More than half of patients with advanced HIV have neuropathy, making it a major area for preventive and symptomatic therapeutic trials.
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peripheral neuropathy cause
It is believed that the virus triggers sensory neuropathy through neurotoxic mechanisms. This reaction has often been unmasked or exacerbated by certain antiretroviral drugs that produce mitochondrial toxicity, which tends to make the neuropathies more frequent and serious.
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neurological trauma numbers
In the United States, an estimated 1.7 million people suffer traumatic head injuries each year, and roughly 52,000 will die. An estimated 265,000 individuals in the United States are living with spinal cord injury.
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neurological trauma cost
Those who survive a brain injury face a lifetime of disability, with economic costs approaching $60 billion annually. The cost of caring for individuals w/ spinal cord injury approaches $10 billion a year.
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treatments for increased brain pressure
Treatments for increased intracranial pressure include the removal of cerebrospinal fluid, hyperventilation to temporarily decrease blood volume, and the administration of drugs to reduce cellular metabolism or to remove water from the injured tissue.moderate
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brain injury meds
No drug for improving outcomes of traumatic brain | injury has yet been approved.
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spinal cord injury meds
Methylprednisolone is the only FDA-approved treatment for spinal cord injury. While there is increasing controversy about the use of this steroid, earlier studies showed efficacy when people with spinal cord injuries received high intravenous doses within eight hours of the injury.
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treatments for reduced cerebral blood flow
Treatments for the injury-induced reduction of cerebral blood flow include the administration of drugs that increase mean arterial blood pressure.
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pain number and cost
Each year, more than 76.2 million Americans suffer chronic, debilitating headaches or a bout with a bad back or the pain of arthritis — all at a total cost of some $100 billion.
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local anesthetics
Historically, the most familiar of these agents was Novocain, which has been used by dentists for years. Lidocaine is more popular today.
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main types of analgesics
(painkillers) nonopioids, opioids, antiepileptic agents, antidepressants
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nonopioids + examples
main type of analgesic. refer to aspirin and related nonsteroidal antiinflammatory drugs, or NSAIDs. Common NSAIDs include ibuprofen and naproxen.
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opioids + examples
main type of analgesic. morphine, codeine. Opioids are the most potent painkillers and are used for severe pain. Opioids, however, have many adverse side effects, such as respiratory depression and constipation, and in some individuals they have a high potential for abuse.
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antiepileptic agnets examples
gabapentin, topiramate
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antidepressants examples
amitriptyline, duloxetine
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neuropathic pain meds
Antiepileptic and antidepressant drugs are useful primarily for neuropathic pain. The best results have been reported with antidepressants that regulate both serotonin and norepinephrine.
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interesting fact about neuropathic pain meds
Interestingly, SSRIs, which selectively affect serotonin, do not help relieve neuropathic pain. (has to include regulation of norepinephrine too)
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pain: topical treatment
topical (skin) application of high doses of capsaicin has recently been approved for some neuropathic pain conditions. This treatment likely kills the sensing portion of pain fibers, but because these nerve fibers will regenerate, treatment needs to be repeated.
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epilepsy numbers
More than 50 million people have epilepsy worldwide, and 85 percent of those cases occur in developing countries. It is estimated that, globally, there are 2.4 million new cases each year
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epilepsy and maturation
it can start at any age
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idiopathic epilepsy cause
Most idiopathic epilepsies probably are due to the inheritance of one or more mutant genes, often a mutant ion channel gene.
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symptomatic epilepsy cause
Most idiopathic epilepsies probably are due to the inheritance of one or more mutant genes, often a mutant ion channel gene.
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generalized epilepsy signs
loss of consciousness and can cause a range of behavioral changes, including convulsions or sudden changes in muscle tone.
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generalized epilspey cause
They occur when there is simultaneous excessive electrical activity over a wide area of the brain, often involving the thalamus and cerebral cortex
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partial epilepsy signs
are characterized by seizures in which the individual maintains consciousness or has altered awareness and behavioral changes. Partial seizures can produce localized visual, auditory, and skin sensory disturbances; repetitive uncontrolled movements; or confused, automatic behaviors.
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partial epilepsy cause
arise from excessive electrical activity in one area of the brain, such as a restricted cortical or hippocampal area.
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new epilepsy treatment
electrical stimulation therapy, was introduced as another option for hard-tocontrol partial seizures. An implanted device delivers small bursts of electrical energy to the brain via the vagus nerve on the side of the neck. While not curative, vagal nerve stimulation has been shown to reduce the frequency of partial seizures in many patients.
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generalized epilspey meds
Generalized epilepsies often are readily controlled by antiepileptic drugs, with up to 80 percent of patients seizure-free with treatment.
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partial epilepsy meds
partial epilepsies are generally more difficult to treat. Often, they can be controlled with a single antiepileptic that prevents seizures or lessens their frequency, but sometimes a combination of these drugs is necessary + surgery
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epilepsy surgery
Surgery is an excellent option for patients with specific types of partial seizures who do not respond to antiepileptic drugs. Electrical recordings of brain activity from patients allow for precise localization of the brain area from which the partial seizures originate. Once this area has been found, neurosurgeons can then remove it. After surgery, most properly selected patients experience improvement or complete remission of seizures for at least several years.
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next gen of antiepilepsy drugs
Identification of the mutated genes underlying epilepsy may provide new targets for the next generation of antiseizure drugs.
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stroke rank
nation’s third leading | cause of death
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stroke meds
use of the clot-dissolving bioengineered drug, tissue plasminogen activator (tPA), is now a standard treatment in many hospitals. This medication opens blocked vessels (often blocked by blood clots) rapidly to restore circulation before oxygen loss causes permanent damage. tPA breaks up the clot. hunGiven within three hours of a stroke, it often can help in limiting the ensuing brain damage.
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stroke numbers
Stroke affects roughly 795,000 Americans a year — | 137,000 of whom die as a result.
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stroke cost
. The total annual costs are | estimated at $73.7 billion.
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stroke age
Stroke often occurs in individuals over 65 years of age, but a third of people who have strokes are younger.
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stroke prevention
Anticoagulant drugs can reduce the likelihood of clots forming, traveling to the brain, and causing a stroke. Controlling risk factors with diet, exercise, and certain drugs may help prevent stroke.
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stroke current treatments
Other specific treatments involving surgery or arterial stents can clear clogs in the arteries of the neck region; these and other treatments targeting heart disease can help prevent a cutoff of blood supply.
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NGF and animals
When infused into the brains of rats, NGF prevented cell death and stimulated the regeneration and sprouting of damaged neurons that are known to die in Alzheimer’s disease. When aged animals with learning and memory impairments were treated with NGF, scientists found that these animals were able to remember a maze task as well as healthy aged rats.
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mad cow disease's other name
bovine spongiform encephalitis. variant Creutzfeldt-Jakob disease (vCJD), known as prion disease, has been linked to mad cow disease.
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Drosophila and engineered antibodies
those modified to carry the mutant human gene for Huntington’s disease are generally too weak and uncoordinated to break out of their pupal case, the way normal insects do. However, when they are treated so that they also express the gene for an anti-HD antibody, all of them emerge as young adults. Furthermore, these treated flies live longer than the untreated ones that do manage to emerge, and the treated ones show less pathology in their brains.
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cell and gene therapy: viruses
Studies in animal models of human diseases have shown that gene transfer vectors can be effective in correcting at least some aspects of neurological disease. At this time, adeno-associated virus (AAV) and lentivirus seem to be the safest and most efficient vectors. These vectors are being used in clinical trials in patients with Parkinson’s and in some rare genetic diseases. Herpes simplex virus and adenovirus vectors have been evaluated in early-stage human trials for treating brain tumors.
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Because many of these diseases involve proteins that misfold and clump abnormally, lasers are used to measure whether proteins are clumped inside cells that have been robotically distributed into tiny containers, along with the small molecules to be tested. A machine then scans the containers and reports whether particular drugs have changed the protein clumping.
read
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RNA treatments
A new class of potential drugs is based on removing the RNAs that code for the proteins that are causing damage. Mouse models of Huntington’s disease and ALS appear to have responded positively to such treatments, which are delivered via gene therapies.
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medial temporal region vs cortical regions
Whereas the medial temporal region is important for forming, organizing, consolidating, and retrieving memory, it is the cortical areas that are important for long-term storage of detailed knowledge about facts and events and how this knowledge is used in everyday situations.
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how many genes does each cell contain?
The exact number of human genes is uncertain and the functions of many genes are still unknown, but the current estimate is that humans have approximately 20,000–25,000 pairs of genes
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when does migration occur?
Once neural induction has occurred, the next step for new neurons is a journey to the proper position in the brain. This process is called migration, and it begins three to four weeks after a human baby is conceived.
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oldest known human
The oldest known human, Jeanne | Calment, kept her wits throughout her 122-year life span.
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dementia numbers
Together, the dementias affect as many as 6.8 million people in the U.S, and at least 1.8 million of those cases are severe.
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It is also becoming clear that the aging brain is only as resilient as its circuitry. when the circuitry begins to break down, remaining neurons can adapt by expanding their roles, and larger portions of the brain can be recruited so that older people can reach performance levels similar to those of younger adults.
read
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enriching environments: middle vs old aged rats
Middle-aged rats exposed to such environments formed more and longer dendrite branches in the cerebral cortex than did rats housed in isolated conditions. In response to enriched environments, older rats tend to form new dendrite outgrowths and synapses, just as younger animals do. But the response is more sluggish and not as large. Compared with younger rats, older rats have less growth of the new blood vessels that nourish neurons.
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rats and acrobatic training
Another study showed that when rats were given acrobatic training, their brain cells had more synapses per cell than rats given only physical exercise or rats that were inactive. These findings led scientists to conclude that motor learning generates new synapses.
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physical exercise and the brain
Physical exercise alone, however, improved blood circulation in the brain. In humans, aerobic exercise can also improve cognitive performance.
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zebrafish and research
Zebrafish, whose fertilized eggs are transparent, have turned out to be good models for developmental neuroscience research.
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sea slugs and research
Sea slugs have proven to be important in the study of learning and memory.
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Carlsson
Knowledge about another neurodegenerative disease, Parkinson’s disease, has emerged through studies with rabbits and mice. These experiments, conducted by Nobel Laureate Arvid Carlsson, revealed that the neurotransmitter dopamine was being depleted.
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development of levodopa
Using pigeons, scientists then discovered that dopamine was highly concentrated in the basal ganglia, the part of the brain involved in motor function. From there, researchers concluded that Parkinson’s disease causes cells in the basal ganglia to die, limiting the production of dopamine. This finding led to the discovery of the first treatment for Parkinson’s — a drug called levodopa, which is converted to dopamine in brain cells.
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animals and addiction research
Further studies (w/ rats) showed that the part of the brain affected by drugs is the reward pathway, especially the dopamine neurons of the ventral tegmental area, which communicates with the nucleus accumbens. As shown in rats — and consistent with what happens in humans — this pathway is also activated by natural rewards, such as food, water, and sex, but drugs of abuse can take over the reward system by mimicking or blocking the function of neurotransmitters.
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Kandel
In his work on learning and memory, Nobel Laureate Eric Kandel began his investigations using mammals, but soon found they were too complex to enable him to study basic memory processes. So he turned to a simpler organism — the sea slug. After demonstrating that both short- and long-term memory in sea slugs involve the synapse, Kandel was able to illustrate that similar mechanisms are at work in mice and other mammals.
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Kandel's findings
Kandel found that certain stimuli resulted in a more robust protective reflex, a form of learning for the sea slug. Furthermore, the strengthened reflex could remain in place for days and weeks as a short-term memory. Additional work showed that a stronger synapse was responsible for the retention of this information. Long-term memories form in a different way. Stronger stimuli activate genes, resulting in an increase of some proteins and a decrease in others. These changes ultimately lead to the growth of new synapses.
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Hubel
Animal studies led to the understanding of the concept of critical periods in the development of vision. Experiments with monkeys and cats helped determine that treatment for amblyopia. These animal studies showed the importance of the critical period in modifying visual circuits, leading to the realization that there is currently no cure for amblyopia in adults. For this work, neuroscientists David Hubel and Torsten Wiesel won the Nobel Prize in 1981.
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Wiesel
Animal studies led to the understanding of the concept of critical periods in the development of vision. Experiments with monkeys and cats helped determine that treatment for amblyopia. These animal studies showed the importance of the critical period in modifying visual circuits, leading to the realization that there is currently no cure for amblyopia in adults. For this work, neuroscientists David Hubel and Torsten Wiesel won the Nobel Prize in 1981.
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future amblyopia treatment
More recently, studies with mice are starting to reveal what factors change in the brain to prevent rewiring after a certain age. Modifying or removing these factors seems to allow for changes in vision later in life. This has been borne out in the lab, where vision has been restored in older amblyopic mice.
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electrophysiology and diagnosis
hearing loss: This function is assessed in infants through electrophysiological recordings of auditory brainstem responses to sound. During this procedure, electrodes are placed on specific parts of the head, which make recordings that are then processed by a computer. The computer makes an analysis based on the time lapse between stimulus and response. It then extracts this information from background activity.
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MRI length and machine
15-minute MRI procedure, a patient lies inside a massive, hollow, cylindrical magnet and is exposed to a powerful, steady magnetic field.
219
how many disorders have a genetic basis ?
More than 7,000 disorders, including many that affect the brain and neurodevelopment, are suspected to have a genetic basis.
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mental illness and genetics
people missing a certain segment of chromosome 22, due to 22q deletion syndrome, have a higher chance of developing mental illness. However, not all people with this chromosome deletion develop mental illness, nor do all people with mental illness have such a genetic finding.
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intellectual disability and genetics
Many forms of intellectual disability, previously referred to as mental retardation, are also due to genes that are not working properly. Gene mapping enabled doctors to find the FMR1 gene, which is abnormal in people diagnosed with fragile X syndrome, the most common cause of inherited intellectual disability in males. FMR1 is located on the X chromosome and is important for neuronal communication.
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autism and chromosome
Chromosome abnormalities identified through microarray technology have also been associated with autism. Deletions of a certain portion of chromosome 16 can lead to a variety of neurological symptoms, including autism in some individuals. However, at this point in time no one gene or set of genes can be attributed to the majority of autism diagnoses.
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"next generation" sequencing example
this next generation of sequencing has already led to the identification of the MLL2 gene responsible for Kabuki syndrome
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When you look at a scene with both eyes, the objects to your left register on the right side of the retina. This visual information then maps to the right side of the cortex. The result is that the left half of the scene you are watching registers in the cerebrum’s right hemisphere. A similar arrangement applies to movement and touch: Each half of the cerebrum is responsible for processing information received from the opposite half of the body.
read
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photoreceptor numbers and types
- 125 million in each human eye. | - 95 percent are rods; 5 percent cones
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blindness cause
Death of photoreceptors in the macula, called macular degeneration, is a leading cause of blindness among the elderly population in developed countries, including the United States.
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visual acuity
Near the center of the gaze, where visual acuity is highest, each ganglion cell receives inputs — via the middle layer — from one cone or, at most, a few, allowing us to resolve very fine details. Near the margins of the retina, each ganglion cell receives signals from many rods and cones, explaining why we cannot see fine details on either side.
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strabismus therapy
Children with strabismus initially have good vision in each eye. But because they cannot fuse the images in the two eyes, they tend to favor one eye and often lose useful vision in the other. Vision can be restored in such cases, but only during infancy or early childhood. Beyond the age of 8 or so, the blindness in one eye becomes permanent. Until a few decades ago, ophthalmologists waited until children reached the age of 4 before operating to align the eyes, prescribing exercises, or using an eye patch. Now strabismus is corrected very early in life — before age 4 — when normal vision can still be restored.
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auditory cortex regions
for most people, the left side is specialized for perceiving and producing speech. Damage to the left auditory cortex, such as from a stroke, can leave someone able to hear but unable to understand language.
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neurons in the auditory cortex
In the auditory cortex, adjacent neurons tend to respond to tones of similar frequency. However, they specialize in different combinations of tones. Some respond to pure tones, such as those produced by a flute, and some to complex sounds like those made by a violin. Some respond to long sounds and some to short, and some to sounds that rise or fall in frequency. Other neurons might combine information from these specialist neurons to recognize a word or an instrument.
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taste bud numbers
Every person has between 5,000 and 10,000 taste buds. Each taste bud consists of 50 to 100 specialized sensory cells.
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taste process
When the sensory cells (of a taste bud) are stimulated, they cause signals to be transferred to the ends of nerve fibers, which send impulses along cranial nerves to taste regions in the brainstem. From here, the impulses are relayed to the thalamus and on to a specific area of the cerebral cortex, which makes us conscious of the perception of taste.
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odorants and their receptors
An odorant acts on more than one receptor, but does so to varying degrees. Similarly, a single receptor interacts with more than one different odorant, though also to varying degrees. Therefore, each odorant has its own pattern of activity, which is set up in the sensory neurons.
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hairy skin areas
In hairy skin areas, some receptors consist of webs of sensory nerve cell endings wrapped around the base of hairs. The nerve endings are remarkably sensitive. They can be triggered by the slightest movement of the hairs.
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touch process
Signals from touch receptors pass via sensory nerves to the spinal cord, where they synapse, or make contact with, other nerve cells, which in turn send the information to the thalamus and sensory cortex.
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itch
Some nociceptors in the skin respond to chemical stimuli that cause itch. Histamine is an example of such a nociceptor, and it can be released in response to certain bug bites or allergies.
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nociceptor types
Different nociceptor subsets produce molecules that are responsible for the response to noxious (i.e., painful) thermal, mechanical, or chemical stimulation. Interestingly, these same molecules respond to plant-derived chemicals, such as capsaicin, garlic, and wasabi, that can produce pain.
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persistent injury
can lead to changes in the nervous system that amplify and prolong the “pain” signal. The result is a state of hypersensitivity in which pain persists and can even be evoked by normally innocuous stimuli. Persistent pain is in many respects a disease of the nervous system, not merely a symptom of some other disease process.
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transmission of pain and itch messages
transmitted to the spinal cord via small, myelinated fibers and C fibers, very small, unmyelinated fibers.
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pain suppression
Pain messages can be suppressed by systems of neurons that originate within the gray matter in the brainstem. These descending systems suppress the transmission of pain signals from the dorsal horn of the spinal cord to higher brain centers.
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pain suppression and chemicals
Some of these descending systems use naturally occurring chemicals, the endogenous opioids, or endorphins, which are functionally similar to morphine. scientists began studying how to deliver opioids into the spine after discovering a dense distribution of opioid receptors in the spinal cord horn; the technique is now common in treating pain after surgery.
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pain and brain regions
One finding is that no single area in the brain generates pain; rather, emotional and sensory components together constitute a mosaic of activity leading to pain. Interestingly, when people are hypnotized so that a painful stimulus is not experienced as unpleasant, activity in only some areas of the brain is suppressed, showing that the stimulus is still experienced. It just doesn’t hurt anymore.
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sleep disorder number
affect up to 70 million people
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sleep disorder cost
$15.9 billion annually
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sleep stages discovery
These stages were discovered in the 1950s through experiments using electroencephalography (EEG) to examine human brain waves. Researchers also measured movements of the eyes and the limbs.
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how long does the 1st REM period last?
10 - 15 min
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sleep cycles thorughout the night
During the night, these cycles of slow wave and REM sleep alternate, with the slow wave sleep becoming less deep and the REM periods more prolonged until waking occurs.
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most common sleep disorder
imsomnia
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narcolepsy rate
1 case per 3,000
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narcolepsy and brain chemistry
the switching mechanisms controlling the transitions into sleep, particularly REM sleep, do not work properly. This problem is due to the loss of nerve cells in the lateral hypothalamus that contain the neurotransmitter orexin (also known as hypocretin).
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narcolepsy: 2 conditions
- hypnagogic hallucination: tend to enter REM sleep very quickly as well and may even enter a dreaming state while still partially awake - cataplexy: They also have attacks of paralysis during which they lose muscle tone — a state similar to what occurs during REM sleep but instead happens while they are awake. attacks can be triggered by emotional experiences, even by hearing a funny joke.
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wakefulness and neurotransmitters
Wakefulness is maintained by several brain systems, each regulating different aspects of this state. Many of the systems are located in the upper brainstem, where nerve cells using the neurotransmitters acetylcholine, norepinephrine, serotonin, and glutamate connect with the forebrain. histamine and orexin are also important
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wakefulness and brain regions
- nerve cells containing orexin are in the hypothalamus. (their laoss causes narcolepsy) - nerve cells containing histamine are also in the hypothalamus - Activation of the thalamus and the basal forebrain by acetylcholine is particularly important in maintaining activity in the cerebral cortex and consciousness.
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non-REM sleep and brain regions
the transmission of information from the senses through the thalamus is curtailed. there is active suppression of arousal systems by a group of nerve cells in the hypothalamus, called the ventrolateral preoptic (VLPO) nucleus.
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non-REM sleep and neurotransmitters
The cells in the VLPO contain the inhibitory neurotransmitters galanin and GABA.
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brain region and sleep disorder
Damage to the VLPO | nucleus produces irreversible insomnia.
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periodicity of REM sleep
The periodic recurrence of REM sleep about every 90 minutes during sleep is thought to be caused by the on-off switching of REM-generating neurons, which produce acetylcholine and glutamate, and REM-suppressive neurons, which produce norepinephrine, serotonin, and GABA.
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circadian system regulation
The circadian timing system is regulated by the suprachiasmatic nucleus, a small group of nerve cells in the hypothalamus that acts as a master clock. These cells express clock proteins, which go through a biochemical cycle of about 24 hours, setting the pace for daily cycles of activity, sleep, hormone release, and other bodily functions. The suprachiasmatic nucleus also receives input directly from the retina, and the clock can be reset by light so that it remains linked to the outside world’s day-night cycle.
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circadian system research
Researchers first identified the clock proteins expressed by the suprachiasmatic nucleus and determined their important roles in sleep by studying the fruit fly Drosophila melanogaster.
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orexin research
recent work using selective stimulation of orexin neurons by artificially inserted receptors sensitive to fiberoptic light pulses — a process referred to as optogenetic stimulation — produces arousal. This arousal is mediated by orexin activation of norepinephrine neurons in the locus coeruleus.
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sleep factors
the longer a person is awake, the greater the likelihood of an increase in sleep-inducing factor(s). Evidence now suggests that one important sleep factor is the inhibitory neurochemical adenosine. With prolonged wakefulness, increasing levels of adenosine are evident in the brain, initially in the basal forebrain and then throughout the cortex. The increased levels of adenosine serve the purpose of slowing down cellular activity and diminishing arousal. Adenosine levels then decrease during sleep.
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sleep and ATP
Brain adenosine may be produced by ATP breakdown in the course of the high brain activity that takes place during wakefulness. studies in animals found that brain ATP levels soared during the initial hours of non-REM sleep. Because ATP is needed to produce adenosine, which is essential for wakefulness, it makes sense that ATP is produced during sleep.
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prolonged stress
as epinephrine and glugocorticoids continue to be released, the consequences can be negative: memory is impaired, immune function is suppressed, and energy is stored as fat.
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glucocorticoid effects
produce an array of effects in response to stress. These include mobilizing energy into the bloodstream from storage sites in the body, increasing cardiovascular tone and delaying long-term processes in the body that are not essential during a crisis, such as feeding, digestion, growth, and reproduction. Some of the actions of glucocorticoids help mediate the stress response, while other, slower actions counteract the primary response to stress and help re-establish homeostasis. also affect food intake during the sleep-wake cycle. also help the body respond to environmental change.
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epinephrine and stress
Over the short run, epinephrine mobilizes energy and delivers it to muscles for the body’s response.
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glucocorticoid release
In response to signals from a brain region called the hypothalamus, the adrenal glands secrete glucocorticoids.
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stress and the immune system
the activity of the immune system is increased by acute stress. Cortisol and epinephrine facilitate the movement of immune cells from the bloodstream and storage organs, such as the spleen, into tissue where they are needed to defend against infection
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effects of acute stress
enhance muscular activity, restore physiological balance, enhances the memory of earlier threatening situations and events, increases the activity of the immune system, and helps protect the body from pathogens.
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animals and chronic stress
Aging rats show impaired neuron function in the hippocampus — an area of the brain important for learning, memory, and emotion — as a result of increased glucocorticoid secretion throughout their lives.
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glucocorticoid overexposure
- weakened muscles, hypertension, atherosclerosis (hardening of the arteries), abdominal obesity, increases number of neurons damaged by stroke - prolonged glucocorticoid exposure before or immediately after birth causes a decrease in the normal number of brain neurons and smaller brain size.
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epinephrine overexposure
- hypertension, atherosclerosis, abdominal obesity - increases the release and activity of body chemicals that cause inflammation, adding to the body’s chronic stress burden. This continual chemical activity can lead to arthritis and accelerated aging of the brain.
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glucocorticoid-induced | immunosuppression
Normally, glucocorticoids rein in the immune system boost brought on by stress. Without this brake, there is an increased chance of autoimmune disorders caused by an overactive immune system. Such autoimmune disorders occur when the body’s immune defenses turn against itself. Then the individual must be treated with synthetic, man-made forms of glucocorticoids (e.g., hydrocortisone and prednisone) in order to keep the immune system in check.
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medial temporal lobe vs cerebral cortex
Whereas the medial temporal region is important for forming, organizing, consolidating, and retrieving memory, it is the cortical areas that are important for long-term storage of detailed knowledge about facts and events and how this knowledge is used in everyday situations.
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declarative memory and brain regions
Studies using functional brain imaging have identified a large network of areas in the cerebral cortex that work together with the hippocampus to support declarative memory. These cortical areas play a distinct role in complex aspects of perception, movement, emotion, and cognition, each of which contributes to the overall experiences captured in declarative memories.
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bending the elbow
involves contraction of the biceps and lengthening of the triceps.
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skilled movements at high speed
started by agonists and stopped by antagonists, thus ensuring that the joint or limb is returned to the desired position.
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activation of a muscle
Activation of a given muscle can open or close the joints that it spans, depending on whether it is a joint flexor (closer) or an extensor (opener). Flexors and extensors work in opposition to each other, causing the contraction of some muscles and the lengthening of others.
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agonist vs antagonist
Muscles that move a joint in an intended direction are called agonists, and those that oppose this direction of movement are antagonists.
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reflexive knee movement
when a physician taps the muscle tendon at the knee, there is a slight stretch of the knee extensor muscles. This slight muscle stretch is “sensed” by receptors in the muscle called muscle spindles. Innervated by sensory fibers, the spindles send information to the spinal cord and brain about the length and speed of the shortening or lengthening of a muscle. This information is used to control both voluntary and involuntary movements. A sudden muscle stretch sends a barrage of impulses into the spinal cord along the muscle spindle sensory fibers. In turn, these fibers activate motor neurons in the stretched muscle, causing a contraction called the stretch reflex.
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evolution of spinal mechanisms
evolved in primitive vertebrates
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cerebellum and movement
- receives direct information from all the sensory receptors in the head and the limbs and from most areas of the cerebral cortex. The cerebellum apparently acts to integrate all this information to ensure smooth coordination of muscle action, enabling us to perform skilled movements more or less automatically - helps us adjust motor output to deal with changing conditions, such as growth, disability, changes in weight, and aging. It tunes motor output to be appropriate to the specific requirements of each new task (ex: picking up full vs empty cup)
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working memory and brain regions
Working memory depends on the prefrontal cortex as well as other cerebral cortical areas. Studies on animals have shown that neurons in the prefrontal cortex maintain relevant information during working memory and can combine different kinds of sensory information when required. In humans, the prefrontal cortex is highly activated when people maintain and manipulate memories. Distinct areas within the prefrontal cortex support executive functions, such as selection, rehearsal, and monitoring of information being retrieved from long-term memory. To serve these functions, the prefrontal cortex also interacts with a large network of posterior cortical areas that encode, maintain, and retrieve specific types of information — visual images, sounds, and words, for example — as well as where important events occurred and much more.
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semantic memory and brain regions
it appears that different cortical networks are specialized for processing particular kinds of information, such as faces, houses, tools, actions, language, and many other categories of knowledge. Studies using functional imaging of normal humans have revealed zones within a large cortical expanse that selectively process different categories of information, such as animals, faces, or words.
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emotional memory and brain regions
The amygdala appears to play an important role in the emotional aspects of memory, attaching emotional significance to otherwise neutral stimuli and events. The expression of emotional memories also involves the hypothalamus and the sympathetic nervous system, both of which support emotional reactions and feelings.
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procedural memory and brain regions
requires processing by the basal ganglia and cerebellum. The cerebellum is specifically involved in motor tasks that involve coordinated timing.
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episodic memory and brain regions
The medial temporal lobe areas are generally believed to serve a critical role in the initial processing and storage of these memories. Studies have shown that different parts of the parahippocampal region play distinct roles in processing “what,” “where,” and “when” information about specific events. The hippocampus links these elements of an episodic memory. The linkages are then integrated back into the various cortical areas responsible for each type of information.
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memory storage research
Researchers studying the sea slug Aplysia californica, for example, can correlate specific chemical and structural changes in relevant cells with several simple forms of memory in the animal.
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LTP and brain regions
LTP occurs prominently in the hippocampus, as well as in the cerebral cortex and other brain areas involved in various forms of memory.
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LTP and animals
studies using genetically modified mice have shown that alterations in specific genes for NMDA receptors or CREB can dramatically affect the capacity for LTP in particular brain areas. What’s more, the same studies have shown that these molecules are critical to memory
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memory storage and brain regions
no single brain center stores memory. Instead, memory is most likely stored in distributed collections of cortical processing systems that are also involved in the perception, processing, and analysis of the material being learned. In short, each part of the brain most likely contributes differently to permanent memory storage.
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nonfluent aphasias brain region
damage to left frontal lobe
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fluent aphasia brain region
damage to left temporal lobe
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nonfluent aphasias example
Broca's aphasia
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fluent aphasia example
Wernicke's aphasia
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word deafnss brain region
damage to superior temporal lobes
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speech gene mutation
rare mutations of a gene called FOXP2 impede learning to make sequences of mouth and jaw movements that are involved in speech, accompanied by difficulties that affect both spoken and written language. The FOXP2 gene codes for a special type of protein that switches other genes on and off in particular parts of the brain. Changes in the sequence of this gene may have been important in human evolution.
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language and brain regions
Functional imaging methods, too, have identified new structures involved in language. Systems involved in accessing the meaning of words appear to be located (in part) in the middle and inferior portions of the temporal lobe. In addition, the anterior temporal lobe is under intense investigation as a site that may participate in some aspect of sentence-level comprehension.
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sensory-motor circuit for speech, where is it
left posterior temporal lobe
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After neurons stop dividing, they form an intermediate zone, where they gradually accumulate as the brain develops. The neurons then migrate to their final destination.
read
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common migation mechanism (process)
The most common guidance mechanism, accounting for about 90 percent of migration in humans, are glia, which project radially from the intermediate zone to the cortex. In this way, glia provide a temporary scaffolding for ushering neurons to their destination. This process of radial migration occurs in an “inside-out” manner; that is, the cells that arrive the earliest (the oldest ones) form the deepest layer of the cortex.
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less common migration mechanism (process)
inhibitory interneurons, small neurons with short pathways usually found in the central nervous system, migrate tangentially across the brain
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growth cone signaling molecule research
Each protein family is smaller in flies or worms than in mice or people, but its functions are quite similar. As a result, it has been possible to use the simpler animals as experimental models to gain knowledge that can be applied directly to humans. For example, the first netrin was discovered in a worm and hown to guide neurons around the worm’s “nerve ring.” Later, vertebrate netrins were found to guide axons around the mammalian spinal cord. Receptors for netrins were
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molecules and autism
molecules coordinate the maturation of the synapse after it has formed so that it can accommodate the changes that occur as our bodies mature and our behavior changes. Defects in some of these molecules are thourhg tot make ppl suscept
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neuron number and maturation
Only about half the neurons generated during development survive to function in the adult. Entire populations of neurons are removed through apoptosis, programmed cell death initiated in the cells.
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myasthenia gravis characteristics
a disease characterized by fatigue and muscle | weakness