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B and Neuro > Alzheimers > Flashcards

Alzheimers Flashcards

1
Q

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

Acute neurodegeneration

A

Stroke

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3
Q

Chronic neurodegeneration

A

Alzheimers, parkinsons etc.

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4
Q

Natural degeneration

A

ageing

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5
Q

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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6
Q

Prevalence

A
  • 50 million worldwide
  • 1 million UK
  • 1 in 14 people aged over 65
  • At current rate – over 1.5 million people in the UK by 2040
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7
Q

Non-modifiable risk factors

A
  • Age
    • Most important risk factor
    • Ageing DOES NOT = Alzheimer’s disease
    • 65-74 yrs – 3%; 75-84 yrs – 17%; over 85 – 32% of population

Biological sex
* x2 as many women over 65 with AD versus men
* Why? Women live longer than men? Links with loss of the hormone oestrogen post-menopause?

Genetics

Family history

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8
Q

Modifiable risk factors

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

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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9
Q

Preventative factors/recommendations?

A
  • Physical activity
    • Healthy diet
    • Social and cognitive engagement
      ○ Data support a relationship
      Biological explanation?
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10
Q

Early stages symptoms

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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11
Q

Early signs

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
  • Changes in personality
    Apathy, indifference, depression
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12
Q

Early Stage 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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13
Q

Middle-Stage 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.

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14
Q

Late Stage AD

A

Lose awareness – surroundings, time

Difficulties in communicating

Changes in physical abilities – walking, swallowing

Vulnerable to infections (especially pneumonia)

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15
Q

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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16
Q

Advanced stages presentation of symptoms

A
  • 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)
17
Q

AD causes

A
  • There is (most probably) not a single cause of Alzheimer’s disease.
    ○ Most likely develops from multiple factors - genetics, lifestyle and environment.
    Majority of cases (99%) of Alzheimer’s disease are NOT hereditary
18
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.
19
Q

Early onset AD

A
  • Caused by gene mutations on chromosomes;
    Chromosome Gene
    1 Presenelin 1 (PS-1)
    14 Presenelin 2 (PS-2)
    21 Amyloid precursor protein (APP)

These genes possess the characteristic of Autosomal dominant inheritance
* If one of these mutated genes is inherited from a parent – person will almost always develop early onset AD

20
Q
  • Late onset AD
A
  • Genetic risk factors involved
    • e.g. Apolipoprotein E (apoE)
      ○ gylcoprotein, transports cholesterol in blood, plays a role in cellular repair
      ○ E4 = one allele of ApoE
      Presence of E4 = increases risk of developing AD (does not cause AD)
21
Q
  • ApoE and b-amyloid
A

Normally – b-amyloid is soluble
* BUT… becomes insoluble when ApoE4 attaches to it
* Therefore, more likely to be deposited in plaques
* Presence of ApoE4
Increases deposits of b-amyloid and formation of plaques

22
Q

Pathology

A
  1. Brain atrophy
  2. Cellular level features
    • Senile plaques
    • Neurofibrillary tangles
  3. Synaptic loss
  4. Selective depletion of neurotransmitter systems (e.g. Ach)
23
Q

Brain atrophy

A

Severe degeneration of the hippocampus, cerebral cortex and ventricular enlargement

24
Q

Cellular level features

A

Normal = is usually short form amyloid beta

AD = increase of long form amyloid beta which are less soluble > lead to accumulation of plaques

Normal = tau binds to and stabilizes microtubules

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

25
Q

Synaptic loss

A
  • Extensive
  • Depletion of selective neurotransmitter systems
    • Acetylcholine (Ach)
    • Glutamate
    • Serotonin
    • Noradrenaline
26
Q
A
27
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 (affecting learning and memory)
28
Q

Treatment - existing and developing treatment

A
  • Psychological
    • For example: external memory aids, visual imagery, reality orientation
  • Pharmacological
    • Cholinesterase inhibitors
    • Glutamate receptor antagonists
29
Q

Psychological (non-pharmacological) approaches treatments

A

Does not stop Alzheimers development but does increase individual’s quality of life

  • Memory Aids
    • diaries, journals, lists,
  • Cognitive Behavioural Therapy (CBT)
    • aimed at reducing depression/anxiety (rather than specifically AD)
  • Music Therapy
    • to help engage and express feelings
  • Structured social interaction
    • Allows a carer to maintain an activity/contact with a patient for 10-15 mins/day
  • Stimulated presence therapy
    • Using reminders of events from their personal life
    • Helps reduce agitation and restlessness
30
Q

Caregiving

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
  • Caregiver wellbeing and burden
    Reduce carer burden/stress and improve quality of lif
31
Q

Pharmacological approaches

A
  • Cholinergic drugs
  • 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
32
Q
  • Glutamate receptor antagonists
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
33
Q
  • Treatment approaches in development
A
  • Strategies to reduce b-amyloid accumulation
    ○ Anti-inflammatory agents
    ○ Enzyme inhibitors (decrease production of b-amyloid)
    • Strategies to reduce tau aggregation
      ○ Anti-inflammatory agents
    • Improving cardiovascular health
34
Q

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
35
Q

Biomarkers specific to AD

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 (*need age comparison)
      ○ Amyloid or Tau PET scans – to examine accumulation of amyloid/tau
      ○ Fluorodeoxyglucose PET scans – to examine energy i.e. glucose, use in brain

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