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

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

Flashcards in Alzheimer’s: Clinical Features, Aetiology and Drug Treatment Deck (45)
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1

Clinical features of typical AD?

- Impaired episodic memory (recent memories, but older memories spared)

- head turning sign (look to family for reassurance/confirmation)

- difficulty following convos

- word-finding issues

2

Anatomical location of dysfunction in impaired episodic memory?

Dysfunction in:

- medial temporal lobe
- hippocampus

3

Clinical features of AD as it progresses?

- increasingly impaired executive function

- increasingly impaired attention

- eventual apraxia

4

Anatomical location of dysfunction in impaired attention in AD

Frontal and parietal atrophy

5

Clinical features of atypical AD?

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

- visuospatial issues (posterior cortical atrophy)

- primary progressive aphasia (asym. left atrophy)

6

Age of onset in atypical AD?

Younger age of onset

7

Define dementia?

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]

8

Most common neurodegenerative dementia?

AD

9

Criteria for DLB?

Cognitive impairment before/within 1 year of PD symptoms

(2nd most common dementia)

10

Define Vascular Dementia?

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

11

Features of Fronto-Temporal Lobar Degeneration (FTLD)?

- behavioural changes
- semantic dementia
- progressive non-fluent aphasia

12

Investigations for AD?

- MMSE/MMSA (Mini Mental State Examination)

- Montreal Cognitive Assessment (MoCA)

- Addenbrookes Cognitive Assessment (ACE)

13

Purpose of neuropsychological assessment?

- tests multiple cognitive domains

- excludes DDx (e.g. depression)

- establishes baseline

14

Structural imaging for AD examples?

- MRI

- CT

- Longitudinal imaging studies

15

What is seen on MRI of AD?

- General atrophy
- hippocampal atrophy

16

Why do an MRI for AD?

Exclude DDxs

17

Functional imaging for AD examples?

- Amyloid PET

- FDG PET

- Tau PET

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

18

AD on CSF analysis results?

Decreased Aβ, increased tau

19

How to definitively diagnose AD?

Brain biopsy or post-mortem

20

Overview of microscopic neuropathology of AD?

- Aβ

- intracellular neurofibrillary tangles (tau)

- neuronal loss

21

Overview of aetiology of AD?

- inflammation
- oxidative stress
- mitochondrial dysfunction
- interaction w/ vascular damage
- amyloid/tau pathology

22

Describe the amyloid hypothesis

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

Risk factors of AD?

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

24

Genetic causes of AD?

- Familial AD (APP, presenilin 1/2)

- APOE (E4- 5x risk homozygote, E2 protective)

- trisomy 21 (100% have AD by 40yrs)

25

Protective risk factors for AD?

- diet

- education (cognitive reserve effect, neuropathology occurs but onset of AD takes longer)

- exercise

26

Relationship between AD pathology and AD symptoms?

Pathology starts 10-20 yrs prior to symptoms/diagnosis

27

Overview of stages of AD development?

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

What is Mild Cognitive Impairment (MCI)?

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

29

Relationship between amnestic and AD?

Amnestic type have increased likelihood of progression to AD

30

Causes of MCI?

AD, depression, hyperthyroidism

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