Many people in Sacramento would like to know what causes their parent's late-onset Alzheimer's disease or increases the risk of it. Now a new gene has been discovered related to late-onset Alzheimer's, for example for people who come down with the disease in their eighties or older.
The study found that individuals with a particular variation in the gene MTHFD1L may be almost twice as likely to develop AD as those people without the variation. But is DNA also destiny? Are you looking for science and health information that is trustworthy? Check out the Public Library of Science (PLoS). The Public Library of Science (PLoS) is a non-profit organization of scientists and physicians committed to making the world's scientific and medical literature a freely available public resource.
What if you lowered your homocysteine levels by nutrition, for example by taking certain bioactive forms of folate, vitamin B 6 and vitamin B12, for example? Would lowering the homocysteine levels be of value in preventing late-stage onset of Alzheimer's disease? After all, high levels of homocysteine are associated with an increased risk factor of developing late-onset Alzheimer's disease.
Or can that gene variation be switched off my some means, such as nutrition or lifestyle changes? If 50 percent of the population eventually gets some form of dementia, is there any way to prevent it once you know you have the gene variation?
According to a September 23, 2010 EurekAlert! news release, "New gene associated with increased risk of Alzheimer's disease," researchers have identified a gene that appears to increase a person's risk of developing late-onset Alzheimer disease (AD), the most common type of the disease.
Abbreviated MTHFD1L, a gene on chromosome six, was identified in a genome-wide association study by a team of researchers led by Margaret Pericak-Vance, Ph.D., director of the John P. Hussman Institute for Human Genomics (HIHG) at the University of Miami Miller School of Medicine. Details appear September 23 in the open-access journal PLoS Genetics.
Check out the study's abstract for the article in PLOS-Genetics, "Dementia Revealed: Novel Chromosome 6 Locus for Late-Onset Alzheimer Disease Provides Genetic Evidence for Folate-Pathway Abnormalities."
The World Health Organization estimates that there are currently 18 million people worldwide with Alzheimer's disease, and this figure is projected to nearly double to 34 million by 2025. By looking at gene variation throughout the human genomes of 2,269 subjects with late-onset AD and 3,107 without the disease, researchers were able to pinpoint small differences in the genetic sequences of people with and without AD.
The study found that individuals with a particular variation in the gene MTHFD1L may be almost twice as likely to develop AD as those people without the variation. But if you have that gene, can you do something about it, such as eat more turmeric or make any type of change at all that might help to switch off the gene or keep it switched off when you reach a certain age referred to as "late stage or late old age?"
"We are hopeful our identification of MTHFD1L as a risk gene for Alzheimer's disease will help us to better understand how this disease develops and potentially serve as a marker for people who may be at increased risk," said co- author Adam Naj, Ph.D, in the September 23, 2010 news release.
"Identifying this gene is important because the gene is known to be involved in influencing the body's levels of homocysteine, and high levels of homocysteine are a strong risk factor for late-onset Alzheimer's disease," said Dr. Pericak-Vance. "In addition, variations of the MTHFD1L gene have been reported to possibly increase the risk of coronary artery disease. Since the function of blood vessels in the brain may affect Alzheimer's disease, this finding may also help us understand how homocysteine levels and blood vessel function in the brain affect Alzheimer's disease."
"By applying the new tools of genomics we are now making rapid progress in finding out what genetic changes are involved in Alzheimer disease. These findings will lead to a better understanding of what's happening in Alzheimer disease, and how we can improve treatments," said Jonathan Haines, Ph.D., Principal Investigator at Vanderbilt University School of Medicine.
"This finding gives us unique insight into possible interactions between genetic and environmental risk factors that contribute to AD," said Joseph Buxbaum, Ph.D., from Mount Sinai School of Medicine in New York and a co-author of the study, according to the Sept. 23, 2010 news release. "We know of environmental and lifestyle factors that can impact homocysteine levels and it will be important to understand whether variations of the MTHFD1L gene can modulate these effects."
The National Institutes of Health National Institute on Aging supported the study (grants AG027944, AG20135, AG19757, AG010491, AG002219, and AG005138); and the National Institute of Neurological Disorders and Stroke (grants NS31153 and NS039764), the Alzheimer's Association, and the Louis D. Scientific Award of the Institut de France.
JDB is the G. Harold and Leila Y. Mathers Professor of Geriatrics and Adult Development. Samples from the National Cell Repository for Alzheimer's Disease (NCRAD), which receives government support under a cooperative agreement grant (U24 AG21886) awarded by the National Institute on Aging (NIA), were used in this study. The authors have declared that no competing interests exist.
The authors of the study are Naj AC, Beecham GW, Martin ER, Gallins PJ, Powell EH, et al. (2010) "Dementia Revealed: Novel Chromosome 6 Locus for Late-Onset Alzheimer Disease Provides Genetic Evidence for Folate-Pathway Abnormalities." PLoS Genet 6(9): e1001130. doi:10.1371/journal.pgen.1001130.
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