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Alzheimer's disease.

Review article
Authors Kaj Blennow
Mony J de Leon
Henrik Zetterberg
Published in Lancet
Volume 368
Issue 9533
Pages 387-403
ISSN 1474-547X
Publication year 2006
Published at Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Pages 387-403
Language en
Keywords Aged, Alzheimer Disease, drug therapy, genetics, physiopathology, Animals, Cholinesterase Inhibitors, therapeutic use, Galantamine, therapeutic use, Humans, Indans, therapeutic use, Male, Molecular Biology, Phenylcarbamates, therapeutic use, Piperidines, therapeutic use, Positron-Emission Tomography, Randomized Controlled Trials, Senile Plaques, enzymology, genetics, pathology, tau Proteins, metabolism, physiology
Subject categories Neurochemistry


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.

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