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Neuroscience and Behaviour > Alzheimers Disease > Flashcards

Alzheimers Disease Flashcards

1
Q

What is Neurodegeneration?

A

‘Progressive damage or death of neurons leading to a gradual deterioration of the bodily functions controlled by the affected part of the nervous system.’

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2
Q

What is acute Neurodegeneration?

A

Stroke

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3
Q

What is Chronic Neurodegeneration?

A

Alzheimer’s Disease, Parkinson’s Disease, Huntington’s Chorea

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4
Q

What is Natural Neurodegeneration?

A

Ageing

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5
Q

What is Disease-induced degeneration?

A

Alzheimer’s disease

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6
Q

What is dementia?

A

An ‘umbrella’ term for a particular group of symptoms

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7
Q

What are the common symptoms of dementia?

A

Characteristic symptoms of dementia = memory, language, problem-solving, other cognitive abilities

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8
Q

What is the most common cause of Dementia?

A

Alzheimer’s disease = most common cause of dementia

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9
Q

What is the Definition of Alzheimers?

A

‘A degenerative brain disorder of unknown origin that causes progressive memory loss, motor deficits, and eventual death.’

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10
Q

How common is Alzheimers in the UK?

A

1 Million, At current rate – over 1.5 million people in the UK by 2040

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11
Q

How common is Alzheimers in the World?

A

50 million worldwide, 1 in 14 people aged over 65

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12
Q

What is the most important risk factor in Alzheimers (non modifiable)?

A

Age -65-74 yrs – 3%; 75-84 yrs – 17%; over 85 – 32% of population

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13
Q

How does Bio sex effect Alzheimers chances?

A

x2 as many women over 65 with AD versus men

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14
Q

What is the Prevelance of AD in 65 and 69 year olds?

A

65-69 years – AD prevalence 0.7% females: 0.6% men

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15
Q

What is the Prevelance of AD in 85 and 89 year olds?

A

85-89 years – AD prevalence 14.2% females: 8.8% males

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16
Q

What is a Modifiable risk factor of Alzheimers disease?

A

Cardiovascular disease risk factors – smoking, diabetes, obesity, hypertension, high cholesterol

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17
Q

What is the Relationship between cardiovascular system and brain function?

A

oxygen and energy supplies
Brain function – reliant on healthy heart and blood vessels
Impaired blood flow = increases risk of dementia/AD

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18
Q

How can you prevent the risk of AD?

A

Physical activity
Healthy diet
Social and cognitive engagement

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19
Q

What are the Early stages of AD?

A

Changes in brain function aren’t sufficient to = symptoms
Compensatory mechanisms activated?
Some changes in brain function (e.g. beta-amyloid levels) may occur up to 20 years before symptoms

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20
Q

What are the Early signs of AD?

A

Normal ageing?
‘Blunting of emotional responses’
Social withdrawal
Memory Impairment
Progressive memory loss (initially episodic and declarative)
Impairment in function
Memory, insight, judgement, language

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21
Q

What is the Presentation of symptoms dependent on?

A

Stage of disease
Age of individual
Sex of individual
Other underlying conditions/medication
Patient vs carer reporting
Access (real or perceived) to diagnosis

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22
Q

What are the Later Stages of AD?

A

Time course varies widely
Onset of symptoms – death ~10 years
Advanced stages
Gross disorientation in time and place
Total dependence on carer for ‘everyday’ tasks
Inability to comprehend/communicate
Little awareness of past or future
Little movement – difficulty in swallowing – infections (e.g. sepsis, pneumonia)

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23
Q

Is there a single cause of Alzheimers?

A

There is (most probably) not a single cause of Alzheimer’s disease. Most likely develops from multiple factors - genetics, lifestyle and environment.

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24
Q

How often is Alzheimers Hereditary?

A

Majority of cases (99%) of Alzheimer’s disease are not hereditary.

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25
Q

What causes brain dysfunction associated with Alzheimer’s?

A

The accumulation of the protein fragment beta‐amyloid (called beta‐amyloid plaques) outside neurons and the accumulation of an abnormal form of the protein tau (called tau tangles) inside neurons are the most prominent brain changes associated with Alzheimer’s.

26
Q

What is Early onset AD?

A

Hereditary
<5% cases
<60 -65 yrs

27
Q

What is Late onset AD?

A

Majority cases
>60-65 yrs

28
Q

What is Autosomal dominant inheritance?

A

If one of these mutated genes is inherited from a parent – person will almost always develop early onset AD (PS -1, PS-2 and APP)

29
Q

What is Apolipoprotein E (apoE)?

A

glycoprotein, transports cholesterol in blood, plays a role in cellular repair

30
Q

What are the three common forms of Alleles in Apolipoprotein E (apoE)?

A

E2, E3, and E4. (*we inherit one form from each parent).

31
Q

What does E4 (allelle of Apolipoprotien E) do?

A

E4 = one allele of ApoE
Presence of E4 = increases risk of developing AD (does not cause AD)

32
Q

what is an allele?

A

different forms of the same gene. Two or more alleles can shape each human trait. Each person receives two alleles, one from each parent. This combination is one factor among many that influences a variety of processes in the body.

33
Q

How does ApoE effect b-amyloid?

A

Normally – b-amyloid is soluble
BUT…becomes insoluble when ApoE4 attaches to it

34
Q

What happens when B- Amyloid is insoluble?

A

it is more likely to be deposited in plaques
Presence of ApoE4 Increases deposits of b-amyloid and formation of plaques

35
Q

What causes B-amyloid accumulation?

A

Head injury, infections, excessive alcohol or other drugs, exposure to toxic substances, lifestyle factors

36
Q

How does AD affect the brain?

A

Brain atrophy - severe degeneration of the hippocampus, cerebral cortex and ventricular enlargement

37
Q

How are cellular level features different.

A

There are senile plaques (amyloid plaques)
- degenerating axon
- mature plaque
-plaque asscociated protien
-degenerating dendrite

38
Q

What does Ab (short form and long form refer to?

A
  • refers to number of amino acids i.e. length of protein – typically 40 (short) or 42 (long)
39
Q

What are some normal cellular level functions?

A

mostly short form, soluble, circulate in CSF/blood

activator of kinase enzymes

protects against oxidative stress

regulation of cholesterol transport
antimicrobial actions

40
Q

What are some different cellular level functions because of Alzheimer’s disease?

A

increased portion of long form

long form – less soluble, more likely to accumulate

induce synaptic dysfunction, disrupt neuronal connectivity and result in neuronal death

weak correlation in quantity and distribution + AD

41
Q

How does tau present in Non- AD brains?

A

tau binds to and stabilizes microtubules (nutrient transport system)

42
Q

How do Neurofibrillary tangles (tau tangles) present in AD brains?

A

tau detaches and sticks to other tau molecules, disrupts cell’s transport system

43
Q

How does synaptic loss present in AD brains?

A

Extensive
Depletion of selective neurotransmitter systems

44
Q

Which neurotransmitter systems become depleted in AD brains?

A

Acetylcholine (Ach)
Glutamate
Serotonin
Noradrenaline

45
Q

Which neurotransmitter systems are more affected?

A

Neurons that use Ach or glutamate are particularly affected
Also, neurons that utilise serotonin or noradrenaline are affected

46
Q

In the Cholinergic hypothesis of AD, what are the properties of Cholinergic neurons?

A

Learning, memory, certain aspects of sleep states

Antagonists (e.g. scopolamine)

Deleterious effect on learning and memory

47
Q

How does AD effect Cholinergic neurotransmission?

A

Degeneration of Ach producing neurons in forebrain

Deficit in Ach producing enzyme

Treatment strategy?

48
Q

What are some examples of Psychological treatment?

A

Memory Aids
Cognitive Behavioural Therapy (CBT)
Music Therapy
Structured social interaction
Stimulated presence therapy

49
Q

What are some examples of Pharmacological treatment?

A

Cholinesterase inhibitors
Glutamate receptor antagonists

50
Q

What types of Cholinergic drugs Boost activity at cholinergic synapses?

A

Aricept, donepezil, rivastigmine, galantamine

51
Q

What is Nearly every drug currently licensed for AD?

A

a cholinesterase inhibitor (ChEI)
eg Ach destruction: Ach Choline and acetic acid

52
Q

How long do Cholinergic drugs
improve clinical symptoms for?

A

for mild to moderate AD, 6-12 months

53
Q

What is a type of Glutamate receptor antagonist?

A

Memantine, a NMDA receptor antagonist

54
Q

How do Glutamate receptor antagonists work?

A

Helps behavioural symptoms such as aggression and agitation

Protects brain cells from toxic effects of excessive levels of glutamate

in moderate-to-severe AD

55
Q

What are some develoing treatment strategies to reduce b-amyloid accumulation?

A

Enzyme inhibitors (decrease production of b-amyloid)

Anti-inflammatory agents

56
Q

What is an example of a developing strategies to reduce tau aggregation?

A

Anti-inflammatory agents

57
Q

What is a biomarker?

A

A naturally occurring molecule, gene, or characteristic by which a particular pathological or physiological process, disease, etc. can be identified

58
Q

Where is a biomarker found?

A

Found in blood, other body fluids, organs and tissues

59
Q

What can biomarkers track?

A

Can track healthy functioning, diagnosis disease, monitor response to treatment, identify health risks (e.g. high cholesterol/high blood pressure for cardiac disease)

60
Q
A

Neuroscience and Behaviour (4 decks)

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