No genetic effect of α1-antichymotrypsin in Alzheimer disease

J. L. Haines, M. L. Pritchard, A. M. Saunders, J. M. Schildkraut, J. H. Growdon, P. C. Gaskell, L. A. Farrer, S. A. Auerbach, J. F. Gusella, P. A. Locke, B. L. Rosi, L. Yamaoka, G. W. Small, P. M. Conneally, A. D. Roses, M. A. Pericak-Vance

Research output: Contribution to journalArticle

92 Scopus citations

Abstract

Alzheimer disease (AD) is the most common neurodegenerative disorder for individuals over the age of 40. AD has a complex etiology, and it is likely that multiple genes, acting independently and/or interacting, affect the risk of developing AD. Several genes involved with AD have been described already, but only the APOE gene on chromosome 19q has been shown to affect the risk of the common late onset form of AD. α1-Antichymotrypsin (AACT) is a major component of the amyloid plaques found in the brains of AD patients, and an allele in its gene has been proposed to increase the risk of developing AD when also associated with the APOE-4 allele. We have examined the role of this AACT polymorphism in a large set of families and sporadic cases, and do not see any effect, either alone or in combination with the APOE-4 allele.

Original languageEnglish (US)
Pages (from-to)53-56
Number of pages4
JournalGenomics
Volume33
Issue number1
DOIs
StatePublished - Apr 1 1996
Externally publishedYes

ASJC Scopus subject areas

  • Genetics

Fingerprint Dive into the research topics of 'No genetic effect of α<sub>1</sub>-antichymotrypsin in Alzheimer disease'. Together they form a unique fingerprint.

  • Cite this

    Haines, J. L., Pritchard, M. L., Saunders, A. M., Schildkraut, J. M., Growdon, J. H., Gaskell, P. C., Farrer, L. A., Auerbach, S. A., Gusella, J. F., Locke, P. A., Rosi, B. L., Yamaoka, L., Small, G. W., Conneally, P. M., Roses, A. D., & Pericak-Vance, M. A. (1996). No genetic effect of α1-antichymotrypsin in Alzheimer disease. Genomics, 33(1), 53-56. https://doi.org/10.1006/geno.1996.0158