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Gene mutation may delay Alzheimer’s up to a decade

September 8, 2015
by Nicole Stempak, Associate Editor
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People with lower levels of inflammation may have a lower risk of developing early-onset Alzheimer’s disease, according to a study published in the journal Molecular Psychiatry.

Neuroscientists at University of California at Santa Barbara found research participants with a gene variation have fully-progressed Alzheimer’s by age 49. Onset is delayed up to 10 years for those with lower levels of the protein eotaxin, which part of the genome that controls inflammation that increases throughout a person’s life.

“We wanted to study those who got the disease later to see if they had a protective modifier gene,” says co-author Kenneth S. Kosik in a news release. Kosik is the co-director of UCSB’s Neuroscience Research Institute and a professor in the Department of Molecular, Cellular and Developmental Biology. “We know they have the mutation. Why are they getting it so much later when the mutation so powerfully determines the early age at onset in most of the family members?”

Lead author Matthew Lalli, who earned his doctorate working in Kosik's Research Group, sequenced the genomes for 117 members of an extended Colombian family with early-onset Alzheimer’s. The Colombian Alzheimer's Prevention Initiative registry comprises more than 4,000 living members from an extended kindred affected with early-onset familial Alzheimer's in Antioquia, Colombia.

“We know that age is the greatest risk factor for Alzheimer’s beyond genetics,” says Lalli, now a postdoctoral fellow at Washington University in St. Louis. “The variant that we found is age-related, so it might explain the actual mechanism of how an increase in age increases the risk of Alzheimer’s—through a rise in eotaxin.”

UCSB researchers replicated the findings by measuring levels of eotaxin in the blood of 150 individuals affected with Alzheimer’s or dementia. They collected DNA samples to confirm who carried the gene variant identified in the Colombian population. Results showed people in the UCSF study with the same viarant had eotaxin levels that did not rise with age. They also experienced a slight delay in the onset of Alzheimer’s.

“If you have that variant, maybe one way to delay or reduce your risk for Alzheimer’s is by genetically holding in check the normal increase in eotaxin that occurs in most of the population,” Kosik says. “Although the gene mutation in the Columbian population is extremely rare, this variant is not. It occurs in about 30 percent of the population, which means it has the potential to protect a lot of people against Alzheimer’s.”