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NMH: Module 2 > Alzheimer’s: Clinical Features, Aetiology and Drug Treatment > Flashcards

Alzheimer’s: Clinical Features, Aetiology and Drug Treatment Flashcards

1
Q

Clinical features of typical AD?

A
  • Impaired episodic memory (recent memories, but older memories spared)
  • head turning sign (look to family for reassurance/confirmation)
  • difficulty following convos
  • word-finding issues
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2
Q

Anatomical location of dysfunction in impaired episodic memory?

A

Dysfunction in:

  • medial temporal lobe
  • hippocampus
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3
Q

Clinical features of AD as it progresses?

A
  • increasingly impaired executive function
  • increasingly impaired attention
  • eventual apraxia
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4
Q

Anatomical location of dysfunction in impaired attention in AD

A

Frontal and parietal atrophy

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5
Q

Clinical features of atypical AD?

A

(may not have episodic memory issues at presentation, but will get later)

  • visuospatial issues (posterior cortical atrophy)
  • primary progressive aphasia (asym. left atrophy)
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6
Q

Age of onset in atypical AD?

A

Younger age of onset

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7
Q

Define dementia?

A

Cognitive issue that impairs function AND affects 2 cognitive domains (1 of which is memory)]- DSM-IV

[NB: dementia is a syndrome- no assumptions on cause]

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8
Q

Most common neurodegenerative dementia?

A

AD

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9
Q

Criteria for DLB?

A

Cognitive impairment before/within 1 year of PD symptoms

2nd most common dementia

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10
Q

Define Vascular Dementia?

A

Dementia w/ step-wise deterioration due to multiple small infarcts (cerebrovascular disease)

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11
Q

Features of Fronto-Temporal Lobar Degeneration (FTLD)?

A
  • behavioural changes
  • semantic dementia
  • progressive non-fluent aphasia
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12
Q

Investigations for AD?

A
  • MMSE/MMSA (Mini Mental State Examination)
  • Montreal Cognitive Assessment (MoCA)
  • Addenbrookes Cognitive Assessment (ACE)
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13
Q

Purpose of neuropsychological assessment?

A
  • tests multiple cognitive domains
  • excludes DDx (e.g. depression)
  • establishes baseline
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14
Q

Structural imaging for AD examples?

A
  • MRI
  • CT
  • Longitudinal imaging studies
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15
Q

What is seen on MRI of AD?

A
  • General atrophy

- hippocampal atrophy

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16
Q

Why do an MRI for AD?

A

Exclude DDxs

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17
Q

Functional imaging for AD examples?

A
  • Amyloid PET
  • FDG PET
  • Tau PET

[NB: no validated Tau ligand, would be useful since tau correlates w/ clinical pathology]

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18
Q

AD on CSF analysis results?

A

Decreased Aβ, increased tau

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19
Q

How to definitively diagnose AD?

A

Brain biopsy or post-mortem

20
Q

Overview of microscopic neuropathology of AD?

A
  • Aβ
  • intracellular neurofibrillary tangles (tau)
  • neuronal loss
21
Q

Overview of aetiology of AD?

A
  • inflammation
  • oxidative stress
  • mitochondrial dysfunction
  • interaction w/ vascular damage
  • amyloid/tau pathology
22
Q

Describe the amyloid hypothesis

A

Increased Aβ accumulation -> tau hyperphosphorylation -> neurofibrillary tangle (NFT)

[NB: tau correlates well w/ cognitive deficits in AD]

1st degree relatives have more than 2x lifetime risk of AD

23
Q

Risk factors of AD?

A
  • age
  • Down’s Syndrome
  • vascular risk (DM, HTN)
  • female >M (2:1)
  • trauma (TBI-> inflammation and increased Aβ)
  • CTE (dementia pugilistica)
24
Q

Genetic causes of AD?

A
  • Familial AD (APP, presenilin 1/2)
  • APOE (E4- 5x risk homozygote, E2 protective)
  • trisomy 21 (100% have AD by 40yrs)
25
Q

Protective risk factors for AD?

A
  • diet
  • education (cognitive reserve effect, neuropathology occurs but onset of AD takes longer)
  • exercise
26
Q

Relationship between AD pathology and AD symptoms?

A

Pathology starts 10-20 yrs prior to symptoms/diagnosis

27
Q

Overview of stages of AD development?

A

Asymptomatic (increased Aβ) -> MCI (even greater Aβ, increased Tau, decreased memory) -> Dementia (A LOT of Aβ, even greater tau, even greater decrease in memory)

28
Q

What is Mild Cognitive Impairment (MCI)?

A

Memory/cognitive issues but no functional impairment (not dementia)

29
Q

Relationship between amnestic and AD?

A

Amnestic type have increased likelihood of progression to AD

30
Q

Causes of MCI?

A

AD, depression, hyperthyroidism

[should we target MCI if this is early AD?]

31
Q

What is subjective cognitive impairment?

A

Subjective memory issue, some will develop MCI

32
Q

Features of pre-clinical AD stage

A
  • normal cognition

- pathogenic biochemical changes (decreased CSF Aβ or increased PET amyloid -> fMRI change)

33
Q

Features of prodromal AD-symptomatic pre-dementia stage

A

Memory loss, +ve AD biomarker

34
Q

Overview of main management for AD?

A
  • give diagnosis
  • behavioural interventions
  • dynamic care plan
  • pharmacological Mx
35
Q

Overview of pharmacological management for AD?

A
  • ACh-esterase inhibitors (Tacrine, Donepezil)
  • NMDA glutamate-r antagonist (Memantine)
  • anti-psychotics (risperidone)
  • monoclonal Ab (aducanumab)

(- nACh-R e.g. galantamine)

36
Q

Cholinergic hypothesis in AD?

A

AD cholinergic denervation of cerebral cortex, esp in temporal lobe

37
Q

Relationship between ACh receptor and AD?

A

musc AChR -> tau phosphorylation

nAChR leads to APP -> Aβ

38
Q

ACh-esterase inhibitor (tacrine) indication and effectiveness in AD?

A

Given to mild-moderate AD

  • small benefit (average increased in 1 MMSE point over 1 yr)
  • no effect on survival
39
Q

NMDA glutamate-R antagonist (memantine) indication and effectiveness in AD?

A

Severe AD or if AChEi not tolerated

  • +1 point on MMSE

[NB: works synergistically w/ AChEi]

40
Q

Anti-psychotic (risperidone) indications in AD?

A

If severely agitated or hallucinations

41
Q

Anti-psychotic (risperidone) side effects?

A
  • decreased cognition
  • PD side effects
  • decreased life expectancy
42
Q

Monoclonal Ab (aducanumab) effectiveness in AD?

A
  • dose-dep response
  • amyloid cleared form CNS but no clinical effect]- given too late?
  • may slow cognitive decline (awaiting phase II results)
43
Q

Monoclonal Ab (aducanumab) side effects?

A
  • oedema

- haemorrhage

44
Q

Overview of “ideal approach” in AD?

A
  • preventative strategies
  • beta-amyloid/tau modification strategies (immunotherapy, enzyme inhib, anti-aggregants, immunotherapy, kinase inhib)
  • symptomatic treatment
45
Q

Sudden deterioration of AD pt- what can we infer?

A

Probs a new condition- atypical symptoms (e.g. UTI)

-> treat by withdrawing/giving medications

NMH: Module 2 (33 decks)

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