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Alzheimer Disease–Related Abnormalities of Amyloid Precursor Protein Isoforms in the Platelet

The Brain's Delegate in the Periphery?

Arch Neurol. 1998;55:1179-1180.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

DURING THE last 5 years, compelling evidence has linked the deposition of -amyloid in the neocortex to the cognitive dysfunction that characterizes Alzheimer disease (AD). The major subunit of AD-related -amyloid is A, a series of approximately 4-kd peptides found as a normal component of all biological fluids, and derived from the processing of a much larger protein, the amyloid precursor protein (APP). Abnormalities of the processing of APP accompany all familial (autosomal dominant) forms of the disease, and transgenic models exhibiting pronounced cerebral -amyloid deposition and some behavioral deficits have been generated by the overexpression of mutant APP. The gene for APP is on chromosome 21, and its overexpression may explain the onset of presenile Alzheimer abnormality that is an invariable complication of Down syndrome. For these reasons, there has been considerable interest in the biochemistry of APP and the possibility that abnormalities of APP processing in the . . . [Full Text of this Article]

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