Only two-sided P-value ≤ 0.01 (ie. LOD scores ≥ 1.4) with markers no more than 25 MB apart in at least two studies were considered. Numbers assigned to linkage studies represent LOD scores. Note that the results by Kehoe et al. (1999) and Lee et al (2004) were not considered here as they were significantly extended in the same groups’ follow-up genome screen (Myers et al. [2002]) and Lee et al [2006], respectively). Only whole-genome studies assessing linkage/association with AD risk, onset age or rate of progression are included. Note that additional studies have been published that performed re-analyses of existing data either by incorporating other variables (such as evidence for AD with and without psychosis [e.g. Bacanu et al, 2002, Avramopoulos et al, 2005, Hollingworth et al, 2007, or parent of origin effects [e.g. Basset et al, 2002].

^a Analyses of these studies are conducted on samples that show partial or complete overlap; these samples include AD families from the Duke Center of Human Genetics (CHG), Joseph and Kathleen Bryan Alzheimer’s Disease Research Center (Bryan ADRC), Indiana Alzheimer’s Disease Research Center National Cell Repository (IADRC), National Institute of Mental Health (NIMH), Vanderbilt University, and University of California Los Angeles (UCLA). Note that each study used distinct marker sets and/or analyses strategies so that none of the entries above actually represent duplicate results; not all of the overlapping samples were used in each study.

^b Only findings of AD sample are considered here.

Please also see disclaimer for more information on this genome screen overview.

References

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