No Genetic Effect of α1-Antichymotrypsin in Alzheimer Disease (original) (raw)

, and spo-Alzheimer disease (AD) is the most common neuroradic late onset AD . The APOEdegenerative disorder for individuals over the age of 4 allele acts in a dose-dependent fashion, with risk in-40. AD has a complex etiology, and it is likely that mulcreasing (and age-at-onset decreasing) with the numtiple genes, acting independently and/or interacting, ber of APOE-4 alleles (Corder et al., 1993), a result affect the risk of developing AD. Several genes inconfirmed in many different populations (Roses et al., volved with AD have been described already, but only 1995). Although the APOE-4 allele is involved in half the APOE gene on chromosome 19q has been shown to of all AD cases (Roses et al., 1996), a substantial numaffect the risk of the common late onset form of AD. ber of individuals with the APOE-4 allele escape AD, a 1 -Antichymotrypsin (AACT) is a major component of and a substantial number of AD cases have no APOEthe amyloid plaques found in the brains of AD patients, 4 allele. This result suggests that other genes may modand an allele in its gene has been proposed to increase ify the effect of the APOE-4 allele. the risk of developing AD when also associated with a 1 -Antichymotrypsin [AACT] has been suspected to the APOE-4 allele. We have examined the role of this play a role in AD since it was first shown to bind the AACT polymorphism in a large set of families and spob-amyloid peptide in AD brains radic cases, and do not see any effect, either alone or . The AACT gene resides on chroin combination with the APOE-4 allele. ᭧ 1996 Academic mosome 14, some 30 cM from the presenilin I gene and Press, Inc. thus is not involved in the early-onset AD linked to chromosome 14. A signal peptide polymorphism (Kamboh et al., 1995) has been described for the AACT gene,