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NEUROLOGY 2006;67:64-68
© 2006 American Academy of Neurology

Exploring the association of glyceraldehyde-3-phosphate dehydrogenase gene and Alzheimer disease

P. I. Lin, MD, PhD, E. R. Martin, PhD, P. G. Bronson, MPH, C. Browning-Large, MS, G. W. Small, MD, D. E. Schmechel, MD, K. A. Welsh-Bohmer, PhD, J. L. Haines, PhD, J. R. Gilbert, PhD and M. A. Pericak-Vance, PhD

From the Center for Human Genetics and Department of Medicine (P.I.L., E.R.M., P.G.B., C.B.-L., D.E.S., J.R.G., M.A.P.-V.) and Department of Psychiatry and Behavioral Sciences (K.A.W.-B.), Duke University Medical Center, Durham, NC, Department of Psychiatry and Biobehavioral Sciences (G.W.S.), University of California, Los Angeles, and Center for Human Genetics Research (J.L.H.), Vanderbilt University Medical Center, Nashville, TN.

Address correspondence and reprint requests to Dr Pericak-Vance, Center for Human Genetics, Department of Medicine, Duke University Medical Center, 595 LaSalle St., Box 3445, Durham, NC 27710; e-mail: mpv{at}chg.duhs.duke.edu

Background: Previous linkage studies have shown that chromosome 12 harbors susceptibility genes for late-onset Alzheimer disease (LOAD). However, association studies of several candidate genes on this chromosome region have produced ambiguous results. A recent study reported the association between the glyceraldehyde-3-phosphate dehydrogenase (GAPD) gene on chromosome 12p and the risk of LOAD.

Methods: The authors conducted family-based and case-control association studies in two independent LOAD data sets on 12 single-nucleotide polymorphisms (SNPs) in the GAPD gene and its paralogs.

Results: No association was found of the GAPD gene with LOAD in the family-based data set, but marginal evidence of association was seen in the later-onset subgroup when age at onset was stratified. The SNP rs2029721 in one GAPD pseudogene was also found to be associated with risk for LOAD in the unrelated case-control data set (p = 0.003).

Conclusions: The GAPD gene and its pseudogene may play a role in the development of late-onset Alzheimer disease. However, the effect, if any, is likely to be limited.

Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the July 11 issue to find the title link for this article.

Supported by NIH NS311530 (J.M.V.), AG021547 (M.A.P.-V.), AG19757 (M.A.P.-V.), AG05128 (M.A.P.-V.), and AG20135 (E.R.M.) grants; a T.L.L. Temple Award (TLL-97-012) and a Zenith Award (ZEN-01-2935) from the Alzheimer's Association (M.A.P.-V.).

Disclosure: The authors report no conflicts of interest.

Received October 7, 2005.

Accepted in final form March 13, 2006.






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