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Abstract
Alzheimer's disease is the most common cause of dementia. Research advances have enabled
detailed understanding of the molecular pathogenesis of the hallmarks of the disease--ie,
plaques, composed of amyloid beta (Abeta), and tangles, composed of hyperphosphorylated
tau. However, as our knowledge increases so does our appreciation for the pathogenic
complexity of the disorder. Familial Alzheimer's disease is a very rare autosomal
dominant disease with early onset, caused by mutations in the amyloid precursor protein
and presenilin genes, both linked to Abeta metabolism. By contrast with familial disease,
sporadic Alzheimer's disease is very common with more than 15 million people affected
worldwide. The cause of the sporadic form of the disease is unknown, probably because
the disease is heterogeneous, caused by ageing in concert with a complex interaction
of both genetic and environmental risk factors. This seminar reviews the key aspects
of the disease, including epidemiology, genetics, pathogenesis, diagnosis, and treatment,
as well as recent developments and controversies.