Abstract
Molecular genetics significantly contributed to the current concepts of the etiology of Alzheimer disease (AD). The genetic association between APOE epsilon4 and both sporadic and familial late-onset AD (LOAD) was discovered almost one decade ago. Soon after this breakthrough it became clear that there should exist additional risk alleles of other genes in order to fully explain the proportion of AD attributable to genetic factors. However, up to now none of the numerous studies involving more than 100 candidate genes revealed convincing evidence for any predisposing risk alleles in genes other than APOE. This review briefly discusses possible reasons for this lack of success and proposes criteria for a more efficient selection of positional and functional candidate genes for LOAD.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Journal of neural transmission (Vienna, Austria : 1996)
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
