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Arch Neurol. 2005;62:1808.

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

The rare families with early-onset Alzheimer disease (AD) and autosomal dominant inheritance have been important in elucidating mutations in the presenilin 1 (PS1) and 2 genes and in the amyloid precursor protein gene that cause disease.¹ These 3 gene mutations underscore the critical importance of normal amyloid precursor protein processing and the fact that a 50% increase in the amount of amyloid- peptide (A₄₂) produced as a result of these mutations is sufficient to cause increased accumulation of A₄₂, which in part causes the early and severe dementia. Abnormal amyloidogenesis is the predominant hypothesis to explain increased A₄₂ burden in the brain of patients with AD and the resultant dementia.¹ Another major unresolved issue in understanding the genetic and molecular basis of AD is the role of Lewy bodies, composed mainly of -synuclein. Brains affected by AD may contain significant levels of Lewy bodies diffusely in neocortical and . . . [Full Text of this Article]

AUTHOR INFORMATION

Roger N. Rosenberg, MD, Editor

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