Genetic Variant Linked to Beta Amyloid Buildup in Alzheimer's
the Psychiatry Advisor take:
A variant in a gene that is associated with the body’s immune system may be linked to increased beta amyloid plaque buildup in Alzheimer’s disease patients and older adults at risk for the neurocogniitve disorder.
Using positron emission tomography imaging in almost 500 people, researchers at the Indiana University School of Medicine examined levels of beta amyloid in the brain and then again two years later. Beta amyloid protein is thought to contribute to Alzheimer’s disease. A genome-wide analysis was then done to find genetic variants associate with a higher rate of plaque accumulation.
Not only was APOE e4, a variant previously identified, found to be associated with higher rates of plaque buildup, but a variant in the IL1RAP gene, which codes for the key immune signaling factor Interleukin-1 Receptor Accessory Protein, had an even more profound effect on amyloid accumulation, the researchers reported in the journal Brain.
The IL1RAP variant was also associated was faster cognitive decline and greater likelihood of progression from mild cognitive impairment to Alzheimer's disease.
“These findings suggest that targeting the IL1RAP immune pathway may be a viable approach for promoting the clearance of amyloid deposits and fighting an important cause of progression in Alzheimer's disease,” Andrew Saykin, PsyD, director of the Indiana Alzheimer Disease Center, said in a statement.
The IL1RAP variant was also associated was faster cognitive decline and greater likelihood of progression from mild cognitive impairment to Alzheimer's.
In a newly published study, a multi-institutional team led by scientists at the Indiana University School of Medicine have discovered an immune system gene associated with higher rates of amyloid plaque buildup in the brains of Alzheimer's patients and older adults at risk for the disease.
The research, reported in the journal Brain, found that a variant in the IL1RAP gene was associated with greater amyloid plaque accumulation over two years and had an even stronger effect than the well-known APOE e4 allele which is notorious for its association with the development of Alzheimer's disease.Using positron emission tomography imaging in nearly 500 individuals, the researchers assessed the levels of brain amyloid deposits at an initial visit and again two years later. A genome-wide analysis was then conducted to identify genetic variants associated with the rate of plaque accumulation during this two-year window.
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