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Alzheimer's disease.

Forskningsöversiktsartikel
Författare Kaj Blennow
Mony J de Leon
Henrik Zetterberg
Publicerad i Lancet
Volym 368
Nummer/häfte 9533
Sidor 387-403
ISSN 1474-547X
Publiceringsår 2006
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi
Sidor 387-403
Språk en
Länkar dx.doi.org/10.1016/S0140-6736(06)69...
Ämnesord 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
Ämneskategorier Neurokemi

Sammanfattning

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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