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Health and Disease > Brain Health and Dementia 1a > Flashcards

Brain Health and Dementia 1a Flashcards

1
Q

What does the Central nervous system (CNS) consist of?

A

Brain
Spinal cord
Retina

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2
Q

What does the peripheral nervous system consist of?

A

Cranial and spinal nerves.

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3
Q

What are motor neurons also known as?

A

Efferent neurons

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4
Q

What are sensory neurons also known as?

A

afferent

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5
Q

Break down the peripheral nervous system.

A

Peripheral Nervous System (cranial and spinal nerves) –> motor –> Somatic / Autonomic.
Autonomic –> Sympathetic / Parasympathetic.

Peripheral Nervous System (cranial and spinal nerves) –> sensory –> sense organs.

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6
Q

What is the peripheral nervous system (PNS) broken down into to?

A

Motor neurons and sensory neurons

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7
Q

What is the motor neurons made up of?

A

Somatic nervous system and Autonomic nervous system

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8
Q

Give some examples of sense organs?

A

Eyes – Sight or Ophthalmoception.
Ears – Hearing or Audioception.
Tongue – Taste or Gustaoception.
Nose – Smell or Olfalcoception.
Skin – Touch or Tactioception.

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9
Q

What is the sensory neuron made up of?

A

Sense organs.

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10
Q

Is the somatic nervous system voluntary or involuntary?

A

voluntary

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11
Q

Is the autonomic nervous system voluntary or involuntary?

A

Involuntary

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12
Q

What does the somatic nervous system include?

A

Skeletal muscles.

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12
Q

What is the somatic nervous system used for?

A

Somatic nervous system is used for things we do consciously such as move a part of our body.

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12
Q

What is the autonomic nervous system made up of?

A

Cardiac and smooth muscle, glands.

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13
Q

What does the autonomic nervous system do?

A

Autonomic nervous system is involuntary and we do not have control over it. Eg, heart beat, contraction of stomach, perspiration.

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14
Q

What is the autonomic nervous system split into?

A

Sympathetic nervous system and parasympathetic nervous system.

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15
Q

What is the function of the sympathetic nervous system?

A

Sympathetic nervous system controls the fight or flight response

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16
Q

What is the function of the parasympathetic nervous system?

A

Parasympathetic nervous system controls the rest and digest process

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17
Q

What does brain stem control

A

cardiac and respiration.

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18
Q

What do the PNS cranial and spinal nerves allow us to do?

A

PNS cranial nerves allows our face to move and our throat to move.

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19
Q

Where is the ventral side of the brain.

A

The bottom

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20
Q

Where is the temporal lobe located?

A

On the side of the brain. The ventral side (bottom).

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21
Q

What is the function of the occipital lobe?

A

Visual information is processed in the occipital lobe. Also responsible for hallucinations. Chronic alcoholism damages this part of the brain and also the rest of the brain. - Alcohol induced hallucinations.

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22
Q

Where is the occipital lobe located?

A

Back of the brain. Called the caudal side. Caudal means back in latin.

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23
Q

What is the parietal lobe responsible for?

A

Responsible for motor function. Where movement is initiated.

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24
Q

Where is the parietal lobe located?

A

Top of the brain. On the dorsal side (the top side).

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25
Q

Where is the frontal lobe located?

A

Rostral side.

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26
Q

Whats the function of the frontal lobe?

A

Processes specific information and cognition and higher function such as social skills, speech and fine movement.

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27
Q

What is the brain composed of?

A
  • Neurons
  • Glial cells (support cells)
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28
Q

What are glial cells?

A

a type of cell that provides physical and chemical support to neurons and maintain their environment.

referred to as “support cells”

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29
Q

What are the four types of glial cells?

A
  • astrocytes (neurochemical support)
  • oligodendrocytes (insulation)
  • microglia (immunology)
  • ependymal cells (secretion)
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30
Q

Are there more neurons or support cells?

A
  • Neurons are outnumbered by support cells
  • 86 billion neurons
  • 860 billion support cells
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31
Q

Function of Oligodendrocyte?

A

Wrap their membranes around the axons.

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32
Q

What is the function of dendrites?

A

the receiving end. THis is where information arrives.
If this info is important enough it will be transferred to the next neuron.

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33
Q

What do the terminals/sinuses do on neurons?

A

transmitting end.

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34
Q

What are ependymal cells?

A

Hairs cilia. Can move to initiate a flow of fluid.

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35
Q

Describe the circulation of the cerebro-spinal fluid (CSF).

A

1) CSF is produced by the choroid plexus of each ventricle.
2) CSF flows through the ventricles and into the subarachnoid space via the median and lateral apertures. Some CSF flows through the central canal of the spinal chord.
3) CSF flows through the subarachnoid space
4) CSF is absorbed into the dural venous sinuses via the arachnoid granulations.

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36
Q

Purpose of lumbar puncture?

A

Collect cerebrospinal fluid to check for infections, inflammation or other diseases. Measure the pressure of cerebrospinal fluid. Inject spinal anesthetics, chemotherapy drugs or other medications

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37
Q

Is their anaesthetic for a lumbar puncture?

A

No anaesthetic for this procedure

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38
Q

Function of the cerebro-spinal fluid (CSF)?

A

Buoyancy
Protection
Homeostasis
Clearing “waste”

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39
Q

What are the physico-chemical properties of cerebral-spinal fluid?

A

Clear
Colourless
Almost similar to plasma

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40
Q

Define buoyancy.

A

allows the brain to float in its own cavity which is the skull. Important for shock absorption. If our brain gets a frontal shock, it would squash at the back. Without it, the brain would get crushed at the back.

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41
Q

What are the main functions of the brain?

A

1- Detects information
2- Processes information
3- Transmits information

For example, detecting danger.

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42
Q

Does the brain process all information?

A

The brain does not process all information. It filters our the information which is not relevant. This filtering is done by the thalamus (the gatekeeper). Stops information if its not important or allows it for further processing if it is important.

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43
Q

What is the direction of transmission of information along several neurons?

A

Left to right

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44
Q

Difference between divergence and convergence?

A

Divergence pathway more random (see diagrams)

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45
Q

Whats a synapse?

A

A connection between two neurons.

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46
Q

What does a synapse transmit across it?

A

electric signals (voltage, current)
chemical signals (neurotransmitters)

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47
Q

What do the vesicles contain?

A

the vesicles are full of neurotransmitters.

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48
Q

Where is a synapse?

A

Where the axon terminal of a transmitting neuron connects to the dendrite of a receiving neuron.

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49
Q

What are synapses described as?

A

Electro-chemical synapse

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50
Q

Function of synapses?

A

Allows transmission of information from one neuron to another

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51
Q

Describe how information is transmitted from one neuron to the next.

A

1) Action potential arrives to axon terminal of transmitting neuron.
2) Information in the form of chemicals or neurotransmitters diffuse across synaptic cleft in vesicles.
3) Vesicles bind to receptor on the receiving neuron.
4) Information continues along next neuron.
5) Process repeats

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52
Q

What is dementia a consequence of?

A

a consequence of neurodegenerative diseases

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53
Q

What is dementia?

A

Dementia describes the pattern of deteriorating intellectual function – particularly (although not
exclusively) in the elderly – that can occur as a result of various neurological disorders.

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54
Q

What are the different types of dementia?

A
  • Alzheimer’s disease
  • Vascular dementia
  • Lewy body disease
  • Frontotemporal dementia (Pick’s disease)
  • Mixed dementia
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55
Q

What is mixed dementia?

A
  • patients suffering with more than one type of dementia at the same time.
    e.g. Alzheimer’s disease and vascular dementia
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56
Q

Is dementia a single condition or a group of conditions?

A

Group of conditions, differs from age-related cognitive decline (ARCD)

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57
Q

Is dementia clinically recongised?

A

Yes it is a clinically recognised syndrome.

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58
Q

Briefly describe the diagnostic process of dementia.

A

step-wise diagnostic process

59
Q

Is dementia the same as age-related cognitive decline (ARCD)?

A

dementia differs from age-related cognitive decline (ARCD).

60
Q

What does dementia cause?

A

impairments in several brain functions

61
Q

What conditions are confused with dementia?

A
  • Age-related cognitive decline (ARCD)
  • Mild cognitive impairment
62
Q

Why is diagnosis of dementia difficult?

A

Diagnosis can be difficult as symptoms in the early stages share similarities with ARCD.

63
Q

Define vascular.

A

Vascular relates to everything which has vessels.

64
Q

What is suspected to be linked to dementia?

A

income

65
Q

What groups of earners have the highest number of people with dementia?

A

Upper middle income and high income

66
Q

Why might upper middle and high income individuals be more likely to develop dementia than low income and lower middle income individuals?

A

Perhaps upper middle income and high income individuals have higher stress jobs, leading to dementia. People with higher income will have better access to drugs/alcohol which are risk factors for dementia.

67
Q

What risk have low income individuals have of developing dementia?

A

Low income seem to be at low risk of dementia compared to other incomes.

68
Q

Where is dementia rising rapidly?

A

Asia and europe

69
Q

What are some Common symptoms of dementia?

A

Lack of motivation (early stages)
Forgetfulness
Losing track of time
Sleep disturbance
Behavioural changes
Unable to recognise familiar people
Reduced mobility (people become confined to their home)
Inability to perform day-to-day tasks (cooking, cleaning, washing, changing clothes)
Relying on permanent care (later stages)

70
Q
A
71
Q

What is the estimated prevalence of Age-related cognitive decline (ARCD)?

A

approx 40% of > 60 years old.

72
Q

What causes age related cognitive decline?

A
  • Changes hormonal levels, enzymatic activity and blood supply to neural tissue.
  • Oxidative damage and genetics are involved, but are not major factors in ARCD.
73
Q

What clinical observations (manifestations) are there of cognitive decline? (what changes occur to the brain because of Age-related cognitive decline)?

A

reduced brain weight/volume
loss of neural bodies (neuron nuclei)
expanded sulci
increased ventricular volume
decreased synaptic density

74
Q

What regions are affected by Age-related cognitive decline?

A
  • Pre-frontal Cortex
  • Medial Temporal Lobe
  • Limbic System (hippocampus)
75
Q

What are the two types of stroke?

A

ischemic and hemorrhagic

76
Q

What does a stroke cause?

A
  • A stroke can induce short- and
    long-term consequences.
  • Vascular dementia can result from a stroke.
77
Q

What causes an ischaemic stroke?

A

Caused by atherosclerosis - plaque blocks blood vessel and stops the flow of blood, depriving the brain of oxygen, causing stroke. This is why its called ischemic.

78
Q

What causes a hemorrhagic stroke?

A

Pressure builds up in the artery wall and blood leaks out causing stroke.

79
Q

What percentage of patients develop vascular dementia after a stroke?

A

Occurs in ~25-30% of patients after a stroke

80
Q

What are the symptoms of vascular dementia?

A

impaired judgment
loss of memory (less severe than Alzheimer’s)
problems with abstract thinking
problems with speech (forgetting simple words)
issues with orientation (objects, time, space)
difficulties in planning and performing familiar tasks
changes in personality, mood, &/or behaviour
loss of initiative
slowness

81
Q

What does Lewy body diseases and parkinsons diseases affect?

A

can affect both motor control and memory

82
Q

How do you distinguish between whether a diseases is Lewy body disease or Parkinson disease?

A

if memory issues occur first –> “Lewy body disease”
if motor issues occur first –> “Parkinson disease”

83
Q

When do most common symptoms of parkinsons occur?

A

most common symptom during advanced stages = hallucinations motor control issues start as hand tremors.

84
Q

What is Lewy body disease & Parkinson’s disease associated with?

A

Associated with:
slow deterioration in social behaviour
problems using language
intellectual impairment
personality change

85
Q

What are the metabolisms like of people who suffer from fronto-temporal dementia?

A

Severe hypo-metabolism

86
Q

What is fronto-temporal dementia also known as?

A

Pick’s disease

87
Q

Whats the cause of fronto-temporal dementia?

A

Causes not well understood (yet?)

88
Q

What cells are affected by fronto-temporal dementia?

A

Neurons responding to dopamine are often affected

89
Q

What is fronto-temporal dementia associated with?

A
  • slow deterioration in social behaviour
  • problems using language
  • intellectual impairment
  • personality change
90
Q

What is Fronto-temporal dementia (Pick’s disease)?

A

a group of disorders that occur when nerve cells in the frontal and temporal lobes of the brain are lost. This causes the lobes to shrink. FTD can affect behavior, personality, language, and movement.

91
Q

Describe the changes to the brain as a result of Fronto-temporal dementia.

A
  • Cortical atrophy contributes to basal ganglia atrophy.
  • Primary pathology affecting basal ganglia causing postsynaptic dopaminergic failure.
  • Certain patterns of cortical and subcortical atrophy may contribute to abnormal behaviours and compulsions such as binge eating.
  • Degeneration of the substantia nigra and nigrostriatal projections causing presynaptic dopaminergic failure.
92
Q

What are some symptoms of Lewy body disease?

A
  • Dementia
  • Hallucinations
  • Cognitive fluctuations
  • Movement disorders
  • Poor regulation of bodily functions
  • Sleep problems
  • Depression
  • Anxiety
  • Apathy
  • Agitation
  • Paranoia
  • Delusions
93
Q

What percentage of dementia cases does Frontotemporal dementia (FTD) make up before 60?

A

It may make up 50% of dementia cases presenting before age 60

94
Q

What determines the symptoms of Frontotemporal dementia (FTD)?

A

The symptoms are related to the anatomic areas affected.

95
Q

What were the clinical syndromes of Frontotemporal dementia (FTD) divided into?

A

“frontotemporal dementia,” “progressive nonfluent aphasia,” and “semantic dementia.”

96
Q

Why might additional symptoms of Frontotemporal dementia (FTD) be found?

A

the pathology may extend beyond the frontal and temporal lobes and additional symptoms may be found.

97
Q

define sporadic.

A

defined as the sudden and unpredictable occurrence of some disease or infection/diseases that are witnessed only occasionally.

98
Q

Are most frontotemporal dementia (FTD) cases sporadic or genetic?

A

most cases are sporadic, some cases are genetic.

99
Q

What is the best known genetic mutations causing FTD?

A

The best-known genetic mutation causing FTD is frontotemporal dementia with parkinsonism.

100
Q

What is frontotemporal dementia with parkinsonism linked to?

A

linked to the microtubule-associated protein tau on chromosome 17.

101
Q

Whats the most common pathology found of FTD?

A

The most common pathology found is frontotemporal degeneration with ubiquitin inclusions.

102
Q

How common is FTD with Pick bodies?

A

FTD with Pick bodies is rare.

103
Q

How is Frontotemporal dementia (FTD) treated?

A

Although there are strategies to help patients and their families, there is no known treatment for the disease.

104
Q

Describe Alois Alzheimer’s investigation?

A
  • Alois Alzheimer was working at the “Asylum for Lunatics and Epileptics”
  • Worked closely with mentally ill patients, associated with old age
  • He performed post-mortem pathologies, and recorded the results:
    1906: brain pathology and symptoms of presenile dementia
    1907: Wrote a paper detailing the disease and his findings
    1910: AD named by Kraepelin as “Alzheimer’s disease”
    1911: Alzheimer’s description of the disease was being widely use
105
Q

What happens in Alzheimer’s disease?

A

The disease damages the brain’s functions:
- memory
- orientation
- calculation

Usually preserves motor functions except in advanced stages.

106
Q

In what age group in Alzheimers predominantly seen in?

A

Predominantly seen in patients > 60 years of age.

107
Q

What problems will a patient experience in the earliest stages of alzheimers disease?

A

short-term memory is affected
patient finds it hard to learn and retain new information
older or distant memory is gradually lost
becomes difficult to recover memories of events and people from earlier life
other symptoms include:
difficulty in putting thoughts into words
difficulty in carrying out simple directed acts
difficulty in recognising well-known faces or objects

108
Q

What changes occur to the brains structure in Alzheimers diseases?

A
  • The hippocampus shrinks noticeably
  • Widening of sulci (arrows on the diagram to the right) and narrowing of gyri.
109
Q

What are the gyri in the brain?

A
  • Gyri are ridges on the surface of the brain, each surrounded by fissures known as sulci.
  • Gyri are unique structures and increase the surface area of the brain (totalling at 2000 cm^2).
  • gyri are typical brain features of “higher species” (primates, cetaceans, ungulates).
110
Q

what are primates?

A

humans, chimpanzees

111
Q

what are cetaceans?

A

whales, dolphins

112
Q

What are ungulates?

A

horses, giraffes

113
Q

Whats the average onset of Alzheimers disease?

A

65 years old

114
Q

Whats the prevalence worldwide of alzheimers disease of 2006?

A

26.6 million worldwide

115
Q

What are the predictions for prevalence of alzheimers diseases globally by 2050?

A

Predictions: 1 in 85 people globally by 2050

116
Q

How does early stages of Alzheimers disease affect a patients day to day routine?

A

In practical terms early Alzheimer’s Disease patients cannot plan meals, manage money, remember to keep doors locked, take medicine on schedule.

AD patient’s may lose their sense of direction and get lost while driving or walking, even in a familiar neighbourhood

117
Q

How does early stages of Alzheimers disease affect a patients mental health?

A

personality changes, anxiety, depression
causes serious problems in relationships.

118
Q

What may patients experience in middle to late stages of alzheimers disease?

A

As AD progresses to middle and late stages the patient may experience:
- delusions
- hallucinations
- Patients may become aggressive or wander away from home if left unsupervised

119
Q

What are some risk factors of alzheimers disease?

A
  • genetic factors can increase the risk of AD
    other people at risk of developing AD
  • history of head trauma (injury)
  • being female
  • lower educational level
120
Q

Describe the continuum of Alzheimers disease.

A

Cognitive function decreases over time (years) and the degree to which it decreases over a certain amount of time determines whether a patients decrease in cognitive function is due to preclinical, MCI, dementia, or simply ageing.

121
Q

What is MCI?

A

Mild cognitive impairment.

122
Q

What are some symptoms of Alzheimers disease?

A
  • Slowly progressive neurodegeneration:
  • initially characterized by impairment of memory
  • subsequently characterized by disturbances in reasoning, planning, language and perception
  • Loss of neurons & synapses in the cerebral cortex and certain subcortical regions:
    –> gross atrophy of the affected regions
  • temporal lobe
  • parietal lobe
  • parts of the frontal cortex
  • cingulate gyrus (limbic cortex)
  • Potential trigger:
    –> increased production or accumulation of beta-amyloid protein
    –> neurotoxic in higher concentrations
123
Q

What is a biomarker?

A

a biomarker is something detectable in the blood/urine in any tissue or any cell that is a sign of a disease. They are used to detect something going wrong early to prevent it from getting worse or to provide a cure.

124
Q

Describe the progression of early stage Alzheimer’s Disease in full.

A
  1. Duration period 2 - 4 years
  2. Frequent memory loss, particularly of recent events
  3. Repeated questions, some problems expressing and understanding language
  4. Writing and using objects become difficult
  5. Depression and apathy can occur
  6. Drastic personality changes may parallel functional decline
  7. Need reminders for daily activities (day-to-day tasks)
  8. Difficulties with sequencing –> impaired driving
125
Q

Describe the second stage of Alzheimer’s Disease in full.

A
  1. Duration 2 - 10 years
  2. Pervasive and persistent memory loss (impacts life across all settings)
  3. Rambling speech, unusual reasoning, confusions (events, time and place)
  4. Potential to become lost in familiar settings
  5. Sleep disturbances
  6. Behavioral symptoms accelerate
  7. Nearly 80% of patients exhibit emotional and behavioral problems which are aggravated by stress and change
  8. Slowness, rigidity, tremors and gait problems  impaired mobility and coordination
  9. Need structure, reminders, and assistance with activities of daily living
126
Q

Describe the third (moderate) stage of Alzheimer’s Disease in full.

A
  1. Increased memory loss and confusion
  2. Problems recognizing family and friends
  3. Inability to learn new things
  4. Difficulty carrying out tasks that involve multiple steps (such as getting dressed)
  5. Problems coping with new situations
  6. Delusions and paranoia
  7. Impulsive behaviour
  8. Morphopathologic manifestations  cerebral cortex
127
Q

Describe the third (severe) stage of Alzheimer’s Disease in full.

A
  1. Duration 1 - 3 years
  2. Confused about past and present
  3. Loss of recognition of familiar people and places
  4. Generally incapacitated
  5. Severe to total loss of verbal skills
  6. Unable to self-care (falling, immobility)
  7. Problems with swallowing, incontinence, and illness.
  8. Extreme problems with mood, behavioural problems, hallucinations and delirium
  9. Patients need total support and care (24/7)
  10. Death
128
Q

Define Aetiology

A

the cause, set of causes, or manner of causation of a disease or condition.

129
Q

What current hypotheses are there on the causes of Alzheimers Disease?

A
  • AD caused by reduced synthesis of acetylcholine
    Multifactorial, involving several pathways:
  • Protein accumulation
  • Plaque formation (Aβ-42) & tangles (hyper-phosphorylated tau)
  • Phospholipid perturbations
  • Inflammation: unregulated activation of glial cells
  • Increased oxidative stress ; decreased anti-oxidant capacity
130
Q

What is amyloid precursor protein?

A

Amyloid precursor protein (APP):
- transmembrane protein
- functions in neuronal growth: survival and repair

131
Q

What is amyloid precursor protein (APP) broken down by?

A

APP is broken down by α, β or γ secretases

132
Q

Describe the amyloid plaque hypothesis.

A

APP is broken down by α, β or γ secretases
During APP degradation, non-soluble peptide fragments (Aβ40, Aβ42) accumulate outside the cell
The non-soluble nature of Aβ-42 helps other protein fragments to build up into plaques.
This is a potential cause of dementia.
Known as the seeding hypothesis.

133
Q

Describe the tau hypothesis.

A

Tau cluster together forming a tangled clump of tau proteins

134
Q

How is Alzheimers disease diagnosed?

A

Neuropsychological, Imaging, Clinical, Post-mortem.

135
Q

Describe the neuropsychological way of diagnosing Alzheimers disease.

A

Mini-mental state examination (MMSE)
–> widely used to evaluate cognitive impairments
Psychological tests for depression
–> depression can be concurrent with AD (early sign of cognitive impairment)

136
Q

Describe the Imaging method of alzheimers disease diagnosis?

A

Computed tomography (CT)
Single photon emission computer tomography (SPECT)
Magnetic resonance imaging (MRI)
Positron emission tomography (PET)

137
Q

Describe the Clinical method of diagnosis of alzheimers disease.

A

Patient history
Collateral history (relatives)
Clinical observations
Presence of characteristic neurological and neuropsychological features
Absence of alternative hypotheses

138
Q

Describe the post mortem method of alzheimers disease diagnosis.

A
  • Histopathological findings (bodies, plaques and tangles)
  • Brain atrophy
139
Q

When can the diagnosis of dementia / alzheimers be confirmed?

A

Although the disease can be diagnosed, you can only confirm the clinical diagnostic of dementia after the death of the individual if the family of the person agree to a post mortem examination of the brain, by identifying taus and amyloid plaques.

140
Q

Is there a cure for dementia?

A

No (not yet?)

141
Q

How can dementia be managed?

A
  • Prevention (genetics, nutrition, pharmacology)
  • Cure (nutrition, pharmacology, psychology)
  • Management (pharmacology, psychology, nutrition)
142
Q

How could genetics be used to prevent dementia?

A

testing genes? genes are a risk factor.

143
Q

How could pharmacology be used to prevent dementia?

A

memory drugs

144
Q

how might dementia be cured with nutrition?

A

nutritional treatment

145
Q

how might dementia be cured by pharmacology?

A

Drugs for abnormal tau.

146
Q

How can dementia symptoms be modulated?

A
  • Short-term treatment with cognitive stimulation

Cholinesterase inhibitors :
- (inhibits acetylcholinesterase from
breaking down acetylcholine)
- Attempts to compensate for neurotransmitter
dysfunction

147
Q

What type of medicine might be best for people with dementia?

A

Personalized medicine which is tailored to the individual based on their status/predicted response or risk.

Health and Disease (26 decks)

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