Alpha-T-Catenin Is Expressed in Human Brain and Interacts With the Wnt Signaling Pathway But Is Not Responsible for Linkage to Chromosome 10 in Alzheimer's Disease

Busby, Victoria, Goossens, Steven, Nowotny, Petra, Hamilton, Gillian, Smemo, Scott, Harold, Denise, Turic, Dragana, Jehu, Luke, Myers, Amanda, Womick, Meredith, Woo, Daniel, Compton, Danielle, Doil, Lisa M., Tacey, Kristina M., Lau, Kit F., Al-Saraj, Safa, Killick, Richard, Pickering-Brown, Stuart, Moore, Pamela, Hollingworth, Paul, Archer, Nicola, Foy, Catherine, Walter, Sarah, Lovestone, Simon, O'Donovan, Michael Conlon ORCID: https://orcid.org/0000-0001-7073-2379, Owen, Michael John ORCID: https://orcid.org/0000-0003-4798-0862, Jones, Lesley ORCID: https://orcid.org/0000-0002-3007-4612, Williams, Julie ORCID: https://orcid.org/0000-0002-4069-0259 and Holmans, Peter Alan ORCID: https://orcid.org/0000-0003-0870-9412 2004. Alpha-T-Catenin Is Expressed in Human Brain and Interacts With the Wnt Signaling Pathway But Is Not Responsible for Linkage to Chromosome 10 in Alzheimer's Disease. Neuromolecular Medicine 5 (2) , pp. 133-146. 10.1385/NMM:5:2:133

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Abstract

The gene encoding alpha-T-catenin, CTNNA3, is positioned within a region on chromosome 10, showing strong evidence of linkage to Alzheimer's disease (AD), and is therefore a good positional candidate gene for this disorder. We have demonstrated that alpha-T-catenin is expressed in human brain, and like other alpha-catenins, it inhibits Wnt signaling and is therefore also a functional candidate. We initially genotyped two single-nucleotide polymorphisms (SNPs) in the gene, in four independent samples comprising over 1200 cases and controls but failed to detect an association with either SNP. Similarly, we found no evidence for association between CTNNA3 and AD in a sample of subjects showing linkage to chromosome 10, nor were these SNPs associated with Abeta deposition in brain. To comprehensively screen the gene, we genotyped 30 additional SNPs in a subset of the cases and controls (n > 700). None of these SNPs was associated with disease. Although an excellent candidate, we conclude that CTNNA3 is unlikely to account for the AD susceptibility locus on chromosome 10.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	MRC Centre for Neuropsychiatric Genetics and Genomics (CNGG) Medicine Neuroscience and Mental Health Research Institute (NMHRI)
Subjects:	R Medicine > R Medicine (General)
Publisher:	Springer Verlag
ISSN:	1535-1084
Last Modified:	04 Mar 2023 03:01
URI:	https://orca.cardiff.ac.uk/id/eprint/81800

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