Molecular pathogenesis of sporadic and familial forms of Alzheimer's disease

William J. Ray, Frank Ashall, Alison M. Goate

Research output: Contribution to journalReview articlepeer-review

43 Scopus citations


Our understanding of the pathogenesis of Alzheimer's disease (AD) comes primarily from the study of rare inherited forms of the disease. Mutations that cause familial AD appear to act by a common mechanism: that of increasing production of Aβ42/43, one of the family of Aβ peptides deposited in senile plaques. However, increased Aβ42/43 production has not been demonstrated to occur in most cases of sporadic AD, suggesting that genetic and environmental factors acting at other stages of the disease process can modify the risk for disease. Such factors most likely include those affecting Aβ aggregation or clearance, the inflammatory response, cerebrovascular disease, or susceptibility of neurons to injury. Identifying these factors will lead to a better understanding of the etiology of the disease and provide additional targets for therapeutic intervention.

Original languageEnglish
Pages (from-to)151-157
Number of pages7
JournalMolecular Medicine Today
Issue number4
StatePublished - 1 Apr 1998
Externally publishedYes


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