Alzheimer’s Disease (60%) = Beta Amyloid And Tau Protein

Question 1

Pathophysiology

Answer 1

Deposition of extracellular 𝛃-amyloid (senile plaques) and intracellular tau protein (neurofibrillary tangles) lead to increased cortical scarring, brain atrophy and reduced cholinergic transmission

Question 2

Clinical features

Answer 2

Steady decline in cognitive function
Memory loss
Cognitive deficits
- aphasia = can’t recognise things
- apraxia = can’t do basic motor skills
- agnostia = can’t talk as well as normal
Visio-special problems
Loss of spontaneously + sense of initiative
Concentration issues
Mood + personality changes
Increased anxiety +/or aggregation
Problems recognising family
Poor sleep

Question 3

Treatment

Answer 3

FIRST LINE: Acetylcholinesterase (AchE) inhibitor
- DONEPEZIL
Severe disease: NMDA antagonist + AchE inhibitor
- MEMANTINE

Question 4

Risk factors

Answer 4

Downs (inevitable and APP gene mutation)
ApoE4 allele in familial Alzheimer’s late onset (V4 cases)

Question 5

What are beta amyloid plaques

Answer 5

Break down product of amyloid precursor protein (APP)