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PH-NE05

Alzheimer's disease

How amyloid plaques and tau tangles build up over many years, why synapses and neurones are lost first in the memory circuits of the medial temporal lobe, and how this produces progressive memory loss and wider decline.

By the end, you can

  • Describe the role of the hippocampus and medial temporal lobe in forming new memories.
  • Explain amyloid-beta plaques and tau tangles and how they relate to synapse and neurone loss.
  • Explain why new memories are affected first and other abilities later.
  • Describe the clinical course and the main complications of advanced disease.
  • Distinguish Alzheimer’s disease from normal ageing and from dementia as a general term.
  • Recognise the classic appearances, staging systems and biomarker tests of Alzheimer’s disease, and explain how cholinesterase inhibitors, memantine and anti-amyloid antibodies act on its mechanism.

What it is

Alzheimer’s disease is a progressive neurodegenerative disease defined by extracellular amyloid-beta plaques and intracellular tau neurofibrillary tangles, with loss of synapses and neurones. It is the commonest cause of dementia, a syndrome of decline in memory and other thinking abilities severe enough to interfere with daily life.

2 types to tell apart
Late onset
Most cases, usually after 65; age is the strongest risk factor, and the APOE ε4 gene variant increases risk.
Early onset
Before 65; a small minority are familial, caused by single-gene mutations (APP, PSEN1, PSEN2), and Down syndrome carries a high risk.

US spelling: ageing → aging.

Normal function

Forming new memories

New facts and events are bound into lasting memories by circuits in the medial temporal lobe: the entorhinal cortex region of the feeds the {{hippocampus}}, which links the elements of an experience together and, over time, helps store them in the wider cortex. The {{fornix}} carries hippocampal output forward.

Memory depends on synapses: their number and strength change with learning. Neurones keep their long axons supplied by transporting cargo along microtubules, which the protein tau stabilises.

With normal ageing, recall may become slower, but new learning and everyday function are preserved.

Point to it on the model