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Neuroscience and Behaviour > Alzheimer's Disease > Flashcards

Alzheimer's 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 are some examples of chronic neurodegeneration?

A
  • Alzheimers disease
  • Parkinsons disease
  • Huntington’s chorea
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3
Q

what is dementia?

A
  • An ‘umbrella’ term for a particular group of symptoms
  • Characteristic symptoms of dementia = memory, language, problem-solving, other cognitive abilities
  • Dementia has many causes
  • Alzheimer’s disease = most common cause of dementia
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3
Q

what is an example of a acute neurodegernation?

A

a stroke

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4
Q

what is Alzheimer’s?

A
  • a disease first identified over 100 years ago
  • a degenerative brain disorder of unknown origin that causes progressive memory loss, motor deficits, and eventual death
  • incidence is high as population ages
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5
Q

what is the prevalence of Alzheimer’s?

A
  • 50 million people affected wordwide
  • 1 million UK
  • 1 in 14 people aged over 65
  • at current rate - over 1.5 million people in the UK by 2024
  • access to diagnosis/treatment/support
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6
Q

Age as a risk factor of Alzheimers disease

A
  • most important risk factor
  • ageing does not mean you have alzheimer’s disease
  • ages 65-74 3% of the population are affected
  • ages 75-84, 17% are affected
  • ages 85 and over, 32% are affected
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7
Q

Biological sex as a risk factor for Alzheimers

A
  • x2 as many women over 65 with AD versus men
  • why? Women live longer than men? Links with the loss of the hormone oestrogen post-menopause
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8
Q

Prevelance of Alzheimers between females and males between the ages of 65-69

A

0.7% female: 0.6% male

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9
Q

Prevelance of Alzheimers between females and males between the ages of 85-89

A

14.2% female
8.8% male

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10
Q

cardiovascular disease as a risk factor for Alzheimer’s disease

A

Relationship between cardiovascular system and brain function:

  • Brain – consumes 20% of the blood’s oxygen and energy supplies
  • Brain function – reliant on healthy heart and blood vessels
  • Impaired blood flow = increases risk of dementia/AD
  • Fatty plaques – cholesterol, salt, age, lack of exercise
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11
Q

what are some things suggested to try to prevent Alzheimers?

A
  • physical activity
  • healthy diet
  • social and cognitive engagement
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12
Q

estimated total cost of dementia care in the UK

A

total cost of dementia care (UK) - £26.3 billion per annum (NHS, private social care, local authority care)

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13
Q

stages of Alzheimers disease (AD)

A

Preclinical AD (no symptoms) → MCI due to AD (very mild symptoms that do not interfere with everyday activities) → Mild (symptoms interfere with everyday activities) → Moderate (symptoms interfere with many everyday activities) → Severe )symptoms interfere with most everyday activities

  • length of each phase of the continuum is influence by age, genetics, gender and other factors
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14
Q

Early symptoms of Alzheimers

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
  • can be seen as normal ages
  • ‘Blunting of emotional responses’
  • Social withdrawal
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15
Q

what are early stage symptoms of AD?

A
  • Temporary memory lapses
  • Forgetting words/names
  • Difficulty performing complex tasks (e.g. at work)
  • Misplacing valuable objects
  • Difficulties with planning/organising
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16
Q

what are middle stage symptoms of AD?

A
  • Forgetful of events/personal history
  • Confuse words
  • Unable to recall personal information
  • Frustration/anger
  • Confusion – surroundings/time
  • Sleep disturbances
  • Bladder/bowel problems
  • Personality/behavioural changes – delusions, paranoia, repetitive (stereotyped) behaviours.
17
Q

Late stage symptom AD

A
  • Lose awareness – surroundings, time
  • Difficulties in communicating
  • Changes in physical abilities – walking, swallowing
  • Vulnerable to infections (especially pneumonia)
18
Q

what % of Alzheimers disease are hereditary?

A

1%

19
Q

what causes brain dysfunction with Alzheimers disease?

A
  • The accumulation of the protein fragment beta‐amyloid (called beta‐amyloid plaques)outsideneurons
  • the accumulation of an abnormal form of the protein tau (called tau tangles)insideneurons are the most prominent brain changes associated with Alzheimer’s.
20
Q

what are the two main types of Alzheimers?

A

Early-onset:
- Hereditary
- diagnosed between 60-65 years of age
- makes up less than 5% of cases

Late-Onset:
- majority of cases
- above the age of 60-65 years

21
Q

what is early onset of AD caused by?

A
  • Caused by gene mutations on chromosomes
  • Autosomal dominant inheritance: If one of these mutated genes is inherited from a parent – person will almost always develop early onset AD
22
Q

causes of late-onset AD

A
  • genetic risk factors involved
  • e.g. Apolipoprotein E (apoE)
23
Q

what is Apolipoprotein E (apoE)?

A
  • gylcoprotein, transports cholesterol in blood, plays a role in cellular repair
  • On chromosome 19, the apolipoprotein E (ApoE) gene has three common forms or alleles: E2, E3, and E4. Thus, the possible combinations in one person* are E2/2, E2/3, E2/4, E3/3, E3/4, or E4/4
  • E4 = one allele of ApoE
  • Presence of E4 = increases risk of developing AD (does not cause AD)
24
Q

what is brain atrophy?

A
  • Loss of connections between neurones
  • severe degeneration of the hippocampus, cerebral cortex and ventricular enlargement of brains in AD patients
25
Q

what are senile plaques?

A
  • extracellular deposits of the amyloid beta protein mainly in the grey matter of the brain
  • Degenerative neuronal elements and an abundance of microglia and astrocytes can be associated with amyloid plaques
26
Q

How is the amyloid beta protein produced?

A

by enzymatic reaction between beta and gamma

27
Q

what are some ‘normal’ functions of amyloid beta peptide?

A
  • mostly short form, soluble, circulate in CSF/blood
  • activator of kinase enzymes
  • protects against oxidative stress
  • regulation of cholesterol transport
  • anti-microbial actions
28
Q

role of amyloid beta peptides in Alzheimers?

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
29
Q

Neurofibrillary tangles (tau tangles) role in Alzheimers

A
  • Non-AD brains – tau binds to and stabilizes microtubules (nutrient transport system)
  • AD – tau detaches and sticks to other tau molecules, disrupts cell’s transport system
30
Q

is synaptic loss extensive in alzheimers disease?

A
  • yes it’s extensive
  • Depletion of selective neurotransmitter systems
    →Acetylcholine (Ach)
    →Glutamate
    →Serotonin
    →Noradrenaline
31
Q

what is cholinergic neurotransmission?

A
  1. acetylcholine production
    acetyl CoA + choline → (with ChAT) Ach and coenzyme A
  2. Acetylcholine destruction
    Ach → (with AchE) Choline and acetic acid
32
Q

Cholinergic hypothesis of AD

A

Cholinergic neurones
- Learning, memory, certain aspects of sleep states
- Antagonists (e.g. scopolamine)
Deleterious effect on learning and memory

Alzheimer’s Disease
- Degeneration of Ach producing neurones in forebrain
- Deficit in Ach producing enzyme
- Treatment strategy? (see next section on ‘treatments)

33
Q

what are some types of psychological treatments for AD?

A
  • memory aids e.g. diaries, journals, lists
  • CBT: aimed at reducing depression and anxiety
  • Music therapy: helps engage and express feelings
  • Structured social interaction: allows carer to maintain an activity/contact with a patient for 10-15 mins a day
  • Stimulated presence therapy: using reminders of events from their personal life
  • helps reduce agitation and restlessness
34
Q

what are caregivers?

A
  • Attending to another person’s health needs and well-being
  • Assisting with activities of daily living
  • Emotional and practical support
  • Managing medications/health service interactions
  • Informal/unpaid
    2/3 = women
    1/3 = over 65 yrs
35
Q

cholinergic drugs as an example of a pharmacological treatment for Alzheimers

A
  • Nearly every drug currently licensed for AD = cholinesterase inhibitor (ChEI)
  • Boosts activity at cholinergic synapses
  • Examples include Aricept, donezepil, rivastigmine, galantamine
  • Licensed (in UK) for mild to moderate AD, transiently improves clinical symptoms for 6-12 months
36
Q

Glutamate receptor antagonists as a pharmacological treatment for Alzheimers disease

A
  • E.g. Memantine
  • NMDA receptor antagonist
  • Protects brain cells from toxic effects of excessive levels of glutamate
  • Licensed (in UK) for treatment of moderate-to-severe AD
  • Shown to temporarily slow the progression of symptoms
  • Helps behavioural symptoms such as aggression and agitation
37
Q

Strategies to reduce beta amyloid accumulation as an Alzheimers treatment

A
  • Anti-inflammatory agents
  • Enzyme inhibitors (decrease production of b-amyloid)
38
Q

Strategies to reduce tau aggression

A

Anti-inflammatory agents

39
Q

what are biomarkers?

A
  • A naturally occurring molecule, gene, or characteristic by which a particular pathological or physiological process, disease, etc. can be identified
  • Found in blood, other body fluids, organs and tissues
  • Can track healthy functioning, diagnosis disease, monitor response to treatment, identify health risks (e.g. high cholesterol/high blood pressure for cardiac disease)
40
Q

What are some biomarkers specific to Alzheimers disease?

A
  • CSF levels/changes of B-amyloid and/or tau
  • Blood tests of brain-derived products
  • Brain imaging studies: MRI/CT – structural changes in brain
  • Amyloid or Tau PET scans – to examine accumulation of amyloid/tau
  • Fluorodeoxyglucose PET scans – to examine energy i.e. glucose use in brain

Neuroscience and Behaviour (27 decks)

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