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.