Medical research has yet to discover an Alzheimer's treatment that effectively slows the disease's progression, but neuroscientists at UC Santa Barbara may have uncovered a mechanism by which onset can be delayed by as much as 10 years.

That mechanism is a gene variant "an allele" found in a part of the genome that controls inflammation. The variant appears to prevent levels of the protein eotaxin from increasing with age, which it usually does hand in hand with inflammation. The findings appear in the journal Molecular Psychiatry.

Lead author Matthew Lalli, who earned his Ph.D. working in UCSB's Kosik Research Group, sequenced the genomes of more than 100 members of a Colombian family affected with early-onset Alzheimer's. These individuals have a rare gene mutation that leads to full-blown disease around age 49. However, in a few outliers, the disease manifests up to a decade later.

"We wanted to study those who got the disease later to see if they had a protective modifier gene," said co-author Kenneth S. Kosik, 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? We hypothesized the existence of gene variant actually pushes the disease onset as much as 10 years later."