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Brief Communications

Nature 405, 531-532 (1 June 2000) | doi:10.1038/35014735

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Neurobiology: Presenilin-1 mutations in Alzheimer's disease

C. Russo1,2, G. Schettini2, T. C. Saido3, C. Hulette4, C. Lippa5, L. Lannfelt6, B. Ghetti7, P. Gambetti1, M. Tabaton8 & J. K. Teller1,9

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Mutations in the gene encoding the protein presenilin-1 are the most common cause of familial Alzheimer's disease1 and they often produce a different disease course from sporadic Alzheimer's and another familial form associated with mutations in the gene encoding beta-amyloid precursor protein2. Here we show that a peculiar form of beta-amyloid that is devoid of the first ten amino acids accumulates in the brains of patients carrying presenilin-1 mutations, and is more abundant than in subjects affected by the other types of Alzheimer's.