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Biopsychology > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

Contribution of Broca and Wernicke to the biological basis of language

A

Paul Broca (1824-1880): Determined that language is lateralized to the left cerebral cortex; He is known for “Tan”, a man who couldn’t speak after having a stroke and was discovered to have a large hole in his left inferior posterior frontal cortex

Carl Wernicke (1849-1905): Suggested that comprehension and speech are regulated by different areas of the left cerebral cortex

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2
Q

***What are the brain regions involved in speech recognition, comprehension, and production?

A

Speech Recognition: Wernicke’s area detects words
Note-auditory cortex detects sounds

Speech Comprehension: Posterior Language Area detects meaning and may house phenomes (parts of words)

Speech Production: Broca’s area finds and sequences words

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3
Q

What brain regions play a role in learning a second language?

A

The same regions used to process the first one (but involves a wider area of activation because your brain is less efficient)

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4
Q

***What is aphasia?

A

A primary disturbance in comprehension or production of speech

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5
Q

***Describe the Neuroanatomy of reading–phonetics vs. whole word reasoning.

A

Reading a word activates a pathway: word > (visual cortex)——–> (Posterior inferior temporal cortex “PIT”)

Sight “whole-word” reading: also activates an object recognition area of the brain (Fusiform cortex)

Phonological reading: also activates the phonological (Wernicke’s area), meaning (Posterior language area) , and articulation (Broca’s area) part of the brain

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6
Q

What brain regions and genes are involved in dyslexia?

What is the concordance rate of dyslexia in identical vs non-identical twins?

A

Brain regions: The following two brain regions do NOT become active when a person who has dyslexia is reading.

  1. ) posterior inferior temporal cortex (PIT)-word recognition
  2. ) fusiform gyrus-whole word reading

Genes:
1.) FoxP2 gene (a transcription factor) >—–>—–> —>—-> —>—>—> alters transcription of a gene called CNTNAP2 (variations of CNTNAP2 are associated with repetitive nonsense word repetition in kids with language disorders)

Concordance rate:
Identical- if one twin has dyslexia, about 90% of the time the other twin has dyslexia.
Non-identical- 30%

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7
Q

***James-Lange theory: describe the sequence and list one problem with this theory

A

Follows this sequence:

  1. (situation in environment “perception”)
    - –>triggers—>
  2. (emotional reaction “autonomic arousal and endocrine responses” + Muscular contractions “Behavior”
    - –>which send feedback to brain to trigger—>
  3. (Subjective Emotion)
    * Feelings are the RESULTS not the Causes of emotional reactions

Problem: The same type of autonomic arousal leads to different emotions

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8
Q

***Cannon-Bard theory

A

Follows this sequence:

  1. (Situation in environment “perception”)
    - –>triggers–>
  2. Processing in brain via the Thalamus
    - –>triggers—>
  3. “Feedback to brain “subjective emotion” —coinciding with but separate from —“Autonomic Arousal”

*subjective feeling of emotion occurs independent of autonomic arousal

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9
Q

***Schachter-singer theory

A

Follows this sequence:
1. (Situation in environment “Perception”)
—>triggers—>
2. “Autonomic Arousal” coinciding with appraisal of current “context”
—>sends feedback to brain to elicit—>
(“subjective emotion”)

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10
Q

What is the evidence supporting the amygdala’s involvement in fear and emotional memory?
What neurotransmitter may reduce amygdala activity?

A

Evidence:
1. Kluver-Bucy Syndrome (1937)-monkeys show no or little fear after removal of the temporal lobes (the amygdala is in the temporal lobes)

  1. Humans with amygdala damage tend to judge unfamiliar faces as more trustworthy and approachable than normal
  2. Perception of fearful faces or unpleasant stimuli increases activity in the amygdala
  3. GABA neurotransmission in the amygdala appears important in reducing fear.
    - older anti-anxiety drugs worked in part by increasing GABA in the amygdala, which had the effect of inhibiting amygdala neurons and decreasing anxiety
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11
Q

Describe the role of the amygdala in emotional memory and implicit prejudice.

A

Emotional Memory:
1. better memory for emotional words associated with greater amygdala activation during learning
Thought Q- If we block amygdala activity immediately after traumatic event, will we prevent PTSD

Prejudice:

1. Even if a person isn't racist, he or she may demonstrated unconscious biases in favor of their own race on a reaction time task
        * Bias on this task is positively correlated with greater amygdala activity.
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12
Q

Describe the relationship between gender, memory, and the left and right amygdala.

A

Men and women encode emotional information using different sides of their amygdala
Women-use left amygdala when learning a set of emotionally arousing pictures
Men- use right amygdala when learning a set of emotionally arousing pictures
Note: men tend to remember emotionally arousing pictures better than women do.

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13
Q

***What evidence supports the role of the mesolimbic dopamine system in pleasure?

A
  1. The mesolimbic dopamine system connects the ventral tegmental area to the nuclues accumbens (the “pleasure center of the brain”)–VTA produces dopamine and releases it into the NAcc
  2. Rats will self-stimulate electrodes located in the VTA and NAcc
  3. All reinforcing stimuli (food, water, sex, drugs) increase dopamine levels in the MDS
  4. Rats no longer self-administer euphoria-producing drugs if the MDS has been damaged
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14
Q

***Explain the role of the cingulate cortex in emotion

A

Cingulate “conflict central”:

  • Monitors conflicts between goals
  • 2 subdivisions
    1. VENTRAL cingulate cortex “VCC”: involved in EMOTIONAL conflicts; connects with amygdala, nucleus accumbens, and hypothalamus
    2. DORSAL cingulate cortex: involved in COGNITIVE conflicts
  • increased cingulate activity in people with anxiety disorders
    * Cingulate damage causes indifference to pain
    * Rarely, it is used to treat depression and anxiety disorders
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15
Q

What are rates of depression in the population?

A
  • Affects 5% (1/20)
  • Increased rate in teens and elderly
  • 16% attempt suicide
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16
Q

What are gender differences in depression?

A

-affects 2x as many women as men

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17
Q

What are genetic contributions to depression?

A
  • More SEVERE depression seems to be more genetic.
  • If parents 1st episode occurs before age of 20, their offspring’s chance of having depression doubles
  • Sibling Concordance rate: 9%
  • Fraternal Twin concordance rate: 11%
  • Identical Twin concordance rate: 40%
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18
Q

***List EACH neurochemical hypothesis of depression

A
  1. ) Depression is due to a lack of Norepinephrine

2. ) Depression is due to a lack of Serotonin

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19
Q

Describe the roles of stress, serotonin, and genes in depression

A

.There are two types of 5HT transporter gene in humans:

1) Long form responds better to cellular signals produced by stress
2) short form: doesn’t respond as well
* **Rates of depression do not differ between people with either form of the gene EXCEPT:
- That stressful life events are more likely to cause depression in people with the short form versus the long form

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20
Q

***How is the hippocampus affected in depression and after stress?

A

.Depression is a very stressful phenomenon, long term elevation of stress related hormones (e.g. cortisol) has been shown to decrease cognitive function and reduce the size of the hippocampus—–therefore, even though evidence is correlational, it is possible that long-term depression can reduce the size of the hippocampus

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21
Q

***What do antidepressant treatments do to the hippocampus?

A

-In tree shrews, reductions in hippocampal size produced by stress are blocked by antidepressant drugs.

In rats, antidepressants and electroconvulsive therapy increases the number of new neurons in the adult hippocampus

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22
Q

***Describe the role of the frontal cortex in depression (Specificaly PFC and ACC)

A

Prefrontal Cortex (PFC):
-Less activationof left PFC in depression
~

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23
Q

How does deep brain stimulation work and is it effective?

A

How does it work?
-Bilateral electrodes are surgically implanted into the ventral cingulate cortex (VCC), and pulse generator placed in clavicle

-Electrodes send very brief stimulation 130x per second

Does DBS work?
-Yes:
After 24 weeks of active DBS, severely depressed patients had significantly reduced scores on the Hamilton Depression Rating Scale and the Beck Depression Inventory; their scores on Global Assessment
When patients were blindly taken off of the DBS, they rapidly relapsed without knowledge that they had been taken off of it.

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24
Q

How many people have schizophrenia and when do individuals with schizophrenia first present with symptoms?

A

1% of world population

Begins in late adolescence or early adulthood

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25
Q

What are symptom clusters of depression?

A

Emotional: Worthless and hopelessness

Somatic: Eating and sleep disturbances, and loss of energy

Cognitive: concentration and memory deficits

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26
Q

What are concordance rates for schizophrenia in fraternal vs. identical twins?

A 
Fraternal = 17%
Identical = 48% (50%)
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27
Q

What is the Rare Variant, common disorder hypothesis?

A

Schizophrenia may be linked to genetic mutations called “Copy Number Variants”.

     - A CNV is a change in the # of whole copies of a gene within an individual genome. 
     - It is predicted that not many people with schizophrenia share the same CNV. 
          * In other words, many rare CNVs can cause a common disease like schizophrenia; but in a given group of people with schizophrenia, you'll find that hardly any share the same CNV that causes their illness.
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28
Q

***What are neuroanatomical differences in individuals with schizophrenia?

A

No single anatomical change distinguishes people with schizophrenia from those without.

Most reliable difference: enlargement of the lateral ventrical
Next most reliable finding: reductions in the size of temporal lobe structures

29
Q

***What are brain activity differences in individuals with schizophrenia?

A

Frontal Cortex does not activate completely during cognitively challenging tasks such as the Wisconsin Card Sort (WCS) task. This task requires that people sort cards based on multiple rules that can shift over time.

***The frontal cortex of people without schizophrenia typically becomes more active during this task

30
Q

***What are developmental influences on schizophrenia?

A

“Neurodevelopmental hypothesis”:
Schizophrenia and the brain dysfunction associated with it are due to problem with brain development

Evidence
1.) gestational complications (e.g., a lack of oxygen)—–>doubles risk

2.) prenatal malnutrition—–>doubles risk

  1. ) Prenatal exposure to flu—–>doubles risk
    * Increased risk in people born 2-3 months after influenza epidemics in Britain and Holland
  2. ) Winter Birth: more people with SCZ are born during winter (58%) than during summer (42%)
31
Q

***What is the dopamine hypothesis and what evidence supports it?

A

Hypothesis: the positive symptoms of schizophrenia are caused by over activity of Dopaminergic synapses in the mesolimbic system, targets the Nucleus Accumbens and amygdala.

Evidence:

  1. ) DA agonists (amphetamine, cocaine,etc) produce psychosis
  2. ) All anti-psychotic drugs block dopamine receptors and many appear to be effective in reducing positive symptoms
    * most researchers agree that the mesolimbic pathway, which includes the amygdala and nucleus accumbens, is involved with SCZ (reinforcement)
32
Q

***What is the Serotonin hypothesis and what evidence supports it?

A

Hypothesis: Schizophrenia results from too much serotonin

Evidence:

  1. ) some Serotonin agonists (LSD) produce hallucinations
  2. ) some anti-psychotics block serotonin receptors (reduce negative symptoms)
33
Q

***What is the Glutamate hypothesis and what evidence is available for it in humans?

A

Hypothesis:
There is too little Glutamate in the brain in SCZ.

Evidence:
Drugs that block glutamate receptors (e.g., PCP) produce all three symptoms in SCZ.

34
Q

Compare Dementia vs. AD

A

Alzheimer’s Disease is a subtype of Dementia. Dementia affects 5% of people over 65yrs—half of those people have AD

35
Q

Is dementia a result of Normal Aging or disease process?

A

??? AD is probably not an inevitable part of aging, but an active disease process

36
Q

How is AD ultimately diagnosed?

A

Diagnosis of AD is confirmed at autopsy by the presence of amyloid plaques and neurofibrillary tangles (NFTs) in the brain

37
Q

***What are plaques?”

A

Plaques are masses of degenerating axons and dendrites that surround a “core” of amyloid (a peptide fragment of amyloid precursor protein or APP.)
“Diffuse plaques”-seen early in the disease process. Neurons near DPs are still alive, but function impaired by the plaque.

“Neuritic plaques”- predominate later in disease course. The amyloid in these plaques is much more densely packed. Neurons near NPs are typically dead.

More plaques in AD than in normal aged brain

38
Q

***What genes affect plaque formation?

A

1.) APP is encoded by a gene on chromosome 21; Some familial, early-onset forms of AD have alterations in this APP gene.
Supports the “faulty APP” hypothesis

2.) Trisomy is an extra copy of chromosome 21. Most people with Down’s syndrome get AD; they have an extra APP gene.
Supports the “too many APP genes” hypothesis
Other forms of early-onset, familial AD have been linked to mutations in two other genes called
3.) presenilin 1
4.) presenilin 2
(PS1 & PS2)
Presenilin proteins form part of the gamma-secretase protease.
Supports the “bad protease” hypothesis

39
Q

What are NFT’s and tau?

A

Neurofibrillary tangles (NFTs): Dead axons and dendrites that end up choking neurons from within

    - they come from tau proteins that normally help to stabilize microtubules
       * In AD, the tau proteins become too sticky or hyper-phosphorylated--->So they clump to one another instead of binding to and stabilizing the microtubule
    - NFTs are found in everyone, but far more in AD
40
Q

What is the relationship between head injury and AD?

A

Head injury doubles the risk of AD
-even if the injury occurred more than 50 years ago (as measured in WWII vets)

Risk of AD increases as severity of injury increases
-vets who were unconscious for more than 24 hours had 4x greater risk for AD

41
Q

***What are the roles of APOE allelic variations in AD?

A

The apolipoprotein E (ApoE) gene = the BEST GENETIC PREDICTOR of Alzheimer’s Disease
(Mutations in APP, PS1, and PS2 genes account for less than 1% of AD cases.)

                  ***ApoE gene Codes for a protein involved in cholesterol breakdown in the bloodstream. - located on chromosome 19. -People carry one of three forms of the gene: E2, E3, and E4; Everyone has two copies or two alleles. *The E4 allele is not good for overall health. Present in 16% of young, 8% in > 65 yrs., and 5% in centenarians. E4 allele is over-represented in AD. In sporadic AD, 33% of people have one E4 allele. In familial, late onset AD, 52% of people with AD have an E4 allele. In the brain, ApoE helps bring together Ab. E4 may be bad at doing this or may bring too much together; either way allowing Ab to accumulate in the brain.
42
Q

***What are drug therapies for AD?

A

1.) Drugs that block the breakdown of acetylcholine (ACh) (by inhibiting acetylcholinesterase) improve memory in AD.

    - Basis for this approach: People with AD lose ACh in cortex and hippocampus due to the degeneration of ACh neurons in the basal forebrain. 
   - Effects: small and don’t last very long (temporarily slow symptoms in mild/moderate AD)
   - ex. Aricept, Exelon, Razadyne
  1. ) NMDA receptor antagonists
    - Basis for this approach: There may be too much glutamate released, which is neurotoxic.
    - Used to treat moderate to severe AD.
    - ex. Namenda
43
Q

Therapy with bad amyloid: How is it supposed to work? Does it work?

A

How is it supposed to work?: Injection of bad amyloid (A-beta 1-42) into a person should, theoretically, boost their immune system to recognize and attack the A-beta 1-42 peptide that they naturally produce (assuming they have the bad gene).

Does it work?: A-beta therapy decreases plaques in some people with mid-stage AD, but it does not improve behavioral outcome (because several neurons have already been impaired or destroyed and it is difficult to create new ones)—->Plaque removal does NOT restore memory.

44
Q

Serotonin and aggression (Ch.10 p. 249-251)

A

Serotonergic neurons play an inhibitory role in aggression and exert a controlling influence on risky behavior (which includes aggression).
Depressed rates of serotonin release (as indicated by low CSF levels of 5-HIAA, which is a metabolite of serotonin (5-HT) are associated with aggression and other forms of antisocial behavior, including assault, arson, murder, and child beating.
*Prozac, an SSRI, helps decrease irritability and aggression

45
Q

Role of the frontal cortex in moral decision making (Ch.10 p. 251-254)

A

When people make judgements that involve conflicts between utilitarian judgements (one person dies but five people live) and personal moral judgements (are you willing to push a man to his death?), the Ventromedial prefrontal cortex is activated. people with damage to the vmPFC display utilitarian moral judgments as they have less of an emotional reaction to these types of dilemmas.
-emotional reactions guide moral judgements as well as decisions involving personal risks and rewards; However, the prefrontal cortex plays a role in suppressing emotional behaviors by helping us to consider the negative consequences.

46
Q

Parkinson’s disease-genes and neurotransmitters (Ch.14 p.375-378)

A

Genes: account for 5% of cases (other 95% are sporatic)

  1. ) mutation of a particular gene on chromosome 4: The gene produces a-synuclein, a protein which is involved in synaptic transmission of dopaminergic neurons—mutation of gene produces a form of a-synuclein that is toxic to the dopaminergic neurons (“toxic gain of function”)
    • very strong: only one has member of the pair of chromosomes has to have a mutated gene for it to produce the toxic substance
  2. Mutation of gene on chromosome 6: the gene produces Parkin, a gene that transports defective or misfolded proteins to organelles that destroy them—-mutation causes loss of function (making it a recessive disorder), which results in the accumulation of of abnormal proteins in dopaminergic neurons, and ultimately results in their death

Neurotransmitters:
Dopamine-Parkinson’s Disease is caused by degeneration of the nigrostriatal system (the dopamine-secreting neurons of the substantia nigra that send axons to the basal ganglia

47
Q

Neurotransmitters and brain regions involved in anxiety disorders and OCD (Ch.15 p. 409-413)

A

Anxiety Disorders
NTs: serotonin (not enough)
Brain regions: amygdala and cingulate, prefrontal, and insular cortices
(ex. increased amygdala and insular activity and decreased vlPFC activity while looking at scary faces)

OCD
NTs: Serotonin (not enough)
Brain regions: Basal Ganglia, caudate nucleus, cingulate gyrus, and prefrontal cortex
-increased activity in caudate nucleus and prefrontal cortex
-infectious illness can lead to abnormalities in basal ganglia which lead to OCD

48
Q

***Causes of autism (Ch.16 p.417-421)

A
  1. ) Heredity: strong evidence for genetic factors-70% concordance rate in monozygotic twins
    • Can be caused by a wide variety of rare genetic mutations, especially those that interfere with neural development and communication

2.) Structural and/or biochemical abnormalities in the brain (20% of cases have biological causes)
-prenatal medical conditions (interfere with development): ex. prenatal thalidomide, maternal infection with rubella, encephalitis caused by herpes virus, tuberous sclerosis
-abnormal brain development during childhood: Abnormally rapid brain growth until the age of 2-3 years (10% larger brains ) and then grow more slowly than brains of unaffected children (by adolescence it is on 1-2% larger than normal); regions of the brain involved in higher-order processes such as communicative functions and interpretation of social stimuli develop more quickly in the autistic brain but then fail to continue to develop normally
*Frontal cortex and temporal cortex grow quickly during first 2 yrs, but slow or stop growing during the next 4 yrs
Three categories of symptoms:
1.) impaired social interaction-ex. brain regions = Fusiform Face Area (FFA) fails to respond to human faces; Superior Temporal Sulcus (STS) and medial prefrontal cortex (mPFC) fail to activate when watching an animation in which they were to accurately express the intentions of the characters
2.) absent or deficient communicative abilities
3.) stereotyped behaviors
-Oxytocin deficiency
-Extreme male brain hypothesis

49
Q

Neurotransmitters and brain regions involved in relapse in substance abuse (Ch.16 p.429-432)

A

NTs: Dopamine and corticotropin releasing hormone (CRH)
Brain Regions:
-medial prefrontal cortex-reduced activity and structural change (cocaine + others)
-cingulate cortex and limbic cortex-decrease in gray matter in methamphetamine and cocaine users
-dorsomedial prefrontal cortex-decreased activation in smokers and gamblers
-decreased gray matter in prefrontal cortex in long time tobacco users

50
Q

***Heritability of substance abuse disorders (Ch.16 p. 438-439)

A

.

51
Q

***List the three theories of where emotions come from.

A
  1. James-Lange theory
  2. Cannon-Bard theory
  3. Schachter-Singer theory
52
Q

Discuss Immediate vs Therapeutic effects of antidepressants

A

.

53
Q

What brain regions are involved in sight or whole-word reading?

A

the posterior-inferior temporal cortex and the fusiform cortex

54
Q

Which of the following lists of brain regions best matches the following list of language functions? Word recognition, word meaning, speech production.

a. ) Wernicke’s area, Broca’s area, Fusiform area
b. ) Wernicke’s area, Posterior language area, Broca’s area
c. Broca’s area, Wernicke’s area, Posterior language area
d. Fusiform, Posterior language area, Wernicke’s area

A

b.) Wernicke’s area, Posterior language area, Broca’s area

55
Q

According to your notes, in general, what are the respective roles of the cingulate cortex, prefrontal cortex, and orbitofrontal cortex in emotional processing?

a. ) representation of goals, conflict detection, sensitivity to rewards and punishments
b. ) sensitivity to rewards and punishments, conflict detection, representation of goal
c. ) Conflict detection, representation of goals, sensitivity to rewards and punishment

A

c.) conflict detection, representation of goals, sensitivity to rewards and punishments

56
Q

Neurochemical imbalances are likely to lead to depression. Which of the following changes in neurotransmitter levels has been strongly implicated in depression?

a. ) There is a decrease in the level of dopamine.
b. ) There is a decrease in the level of norepinephrine.
c. ) There is decrease in the level of serotonin.
d. ) Both b. and c. are correct.
A

d.) Both b. and c. are correct.

57
Q

Which of the following statements is true regarding people with autism?

a. ) The temporal lobe develops at a slower rate in people with autism.
b. ) Increases in childhood immunizations over the last 30 years have been shown to account for the increased rate of autism in the population.
c. ) Studies show that it is unlikely that autism has a genetic basis.
d. ) By 2-3 years of age, the brains of people with autism are, on average, 10 percent larger than normal.

A

d.) By 2-3 years of age, the brains of people with autism are, on average, 10 percent larger than normal.

58
Q

Neurochemical hypotheses of schizophrenia hold that schizophrenia is due to:

a. ) decreases in norepinephrine and serotonin.
b. ) increases in dopamine and serotonin and decreases in glutamate.
c. ) increases in serotonin and norepinephrine and decreases in GABA.
d. ) decreases in dopamine, norepinephrine, and serotonin.

A

b.) increases in dopamine and serotonin and decreases in glutamate.

59
Q

Which of the following is true regarding the relationship between genes and serotonin in depression?

a. ) People with the short-form of the serotonin transporter gene are more likely to be depressed.
b. ) People with the long-form of the serotonin transporter gene are less likely to be depressed.
c. ) All people who suffer childhood maltreatment develop depression.
d. ) People who have the short-form of the serotonin transporter gene are more likely to be depressed if they experienced major stressful life events in the past.

A

d.) People who have the short-form of the serotonin transporter gene are more likely to be depressed if they experienced major stressful life events in the past.

60
Q

In people with schizophrenia, what aspect of brain anatomy is enlarged and what brain region remains somewhat inactive during tasks that normally activate it?

a. ) right prefrontal cortex; left prefrontal cortex
b. ) hippocampus; amygdala
c. ) lateral ventricles; frontal cortex
d. ) cerebellum; hypothalamus

A

c.) lateral ventricles; frontal cortex

61
Q

***What are the symptoms of Broca’s aphasia?

A

Broca’s aphasia: problems with producing speech

  • Use more content words than function words
  • Difficulty with articulation and sound sequence
    e. g., lipstick is likslip
  • Anomia:difficulty finding words
  • Agrammatism: difficulty in using grammar
    e. g., “Son…university…smart…boy…good…good.”
62
Q

***What are the symptoms of Wernicke’s aphasia?

A

Wernicke’s Aphasia: problems with understanding speech

  • Use more function words than content words
  • Cannot recognize spoken words
  • Cannot comprehend the meaning of words
  • Difficulty converting thoughts in to words
63
Q

***Explain the role of the prefrontal cortex in emotion

A

Prefrontal Cortex (goals):

- Left Side-may process info related to positive goals (ex. making money)
- Right Side-may process info related to negative goals (ex. avoiding harm)
64
Q

***Explain the role of the orbitofrontal cortex in emotion

A

Orbitofrontal Cortex (Rewards and Punishments):

- Left Side-Rewards related to our actions
- Right Side-Punishments related to our actions
  • people with damage tend to the OFC tend to make decisions that are impulsive and more risky.
65
Q

***What is evidence for the “Depression is due to a lack of Norepinephrine Hypothesis?”

A

Evidence:
1. Some antidepressant drugs (tricyclics) block NE reuptake into terminals and increase synaptic levels of NE.

  1. Some antidepressants act as monoamine oxidase inhibitors (MAO-I) that prevent MAO breakdown of NE and increase synaptic NE.
66
Q

***What is evidence for the “Depression is dues to a lack of Serotonin (5HT) Hypothesis?”

A

Evidence:

  1. Some antidepressant drugs block NE and 5HT reuptake
  2. All MAO-I antidepressants prevent break down of 5HT by MAO
  3. Selective serotonin reuptake inhibitors (SSRI) block serotonin reuptake and are effective antidepressant drugs for some
  4. Tryptophan (amino acid from which 5HT is formed) depletion produces depression in some subjects
67
Q

What are symptom clusters in schizophrenia?

A

Positive Symptoms: Hallucinations and delusions
Negative Symptoms: flat affect, lack of motivation
Cognitive Symptoms: impaired attention, memory, and thought
-Best predictor of functional status:
*if a person has severe cognitive symptoms they they will struggle MORE with living independently, maintaining social relationships, and keeping a job.

68
Q

***How are plaques made?

A

In AD, the APP is cut too long. (Normal form is 40 amino acids long; peptide referred to as “A-beta1-40” vs. Toxic form is 42 amino acids long peptide; known as “A-beta1-42”

This could be due to:

  1. ) Faulty construction of the APP protein
    - Due to a bad APP gene?
  2. ) An over-production of APP in the brain
    - Due to too many APP genes?
  3. ) A problem with the protease (y-secretase enzyme)
    - Due to a bad protease gene?

Biopsychology (6 decks)

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