| Literature DB >> 19496238 |
Davide Seripa1, Francesco Panza, Marilisa Franceschi, Grazia D'Onofrio, Vincenzo Solfrizzi, Bruno Dallapiccola, Alberto Pilotto.
Abstract
The genetic epidemiology of sporadic Alzheimer's disease (SAD) remains a very active area of research,making it one of the most prolifically published areas in medicine and biology. Numerous putative candidate genes have been proposed. However, with the exception of apolipoprotein E (APOE), the only confirmed genetic risk factor for SAD, all the other data appear to be not consistent. Nevertheless, the genetic risk for SAD attributable to the APOE gene in the general population is 20-0%, providing a strong evidence for the existence of additional genetic risk factors. The first part of the present article was dedicated to non-APOE genetics of SAD, reviewing chromosomes-by-chromosomes the available data concerning the major candidate genes. The second part of this article focused on some recently discovered aspects of the APOE polymorphism and their implications for SAD. An attempt to identify the future directions for non-APOE genetic research in SAD was also discussed.Entities:
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Year: 2009 PMID： 19496238 DOI： 10.1016/j.arr.2008.12.003
Source DB: PubMed Journal: Ageing Res Rev ISSN： 1568-1637 Impact factor: 10.895