While the apolopoprotein E gene has always been suspected as part of the cause, it was "neither necessary nor sufficient to cause AD and as much
as 50 percent of the genetic risk effect remains unexplained," said senior study author Dr Margaret A Perocak-Vance.
In attempt to uncover genetic clues, Perocak-Vance, and her team, completed a comprehensive analysis of 492 late-onset Alzheimer's disease patients and 498 controlled participants.
The technique was powerful enough to detect single nucleotide polymorphisms (SNP), a variation of a single nucleotide of DNA.
Scientists found a new association with a SNP on a chromosome in the brain, which is close to the gene for the vitamin D receptor.
"There is no known connection between this SNP and the vitamin D receptor, but the region between the two is largely uncharacterized, and it is possible that our SNP is in a region that may play some sort of regulatory role," said Dr Jonathan Haines, co-director of the project.
The team also identified four other regions of interest and is furthering their research.
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