Alzheimer’s disease
Progressive neurodegenerative disorder
Projections for AD increase with both time and age. As people live longer, more people are
vulnerable to AD.
Can’t fully diagnose until post mortem.
Profound behavioural and cognitive impairments
Cell loss in multiple brain regions
Symptoms Asking the same Q again and again, forgetting simple things like cooking, losing
ability to play cards, getting lost, neglecting to bathe or change clothes, relying on someone else
to make decisions they previously would have handled themselves, personality changes,
language difficulties, mood swings.
Final Stage: patients lose bladder and bowel control and the ability to chew/swallow. They
become more vulnerable to pneumonia, infection and other illnesses.
Neurofibrillary Tangles
Abnormal proteins wound around each other around neurons. Causes abnormal functioning.
Amyloid Plaques
APP (Amyloid precursor protein) is cut out by certain enzymes at certain sites – leaving beta-
amyloid to congregate to form beta-amyloid plaques. (found by Alzheimer).
- Multiple cell losses.
- Under activity in PET scans.
Causes of Alzhei`11mer’s
- Age: number of people with AD doubles every five years.
- Family History: specific genetic mutations
- Apolipoprotien
Familial Alzheimer’s
Rare form of AD – less than 10% of cases.
Early onset – before the age 65
Caused by mutations on chromosomes 1 (presenelin 1), 14 (presenelin), 21 (amyloid precursor
protein)
Even if only one of these genes is inherited – almost definitely develop early onset AD –
Autosomal Dominant inheritance.
Sporadic Alzheimer’s – Apolipoprotein
APOE associated with late onset.
3 Alleles of APOE gene – 2,3,4
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