New Research Shows Alzheimer’s-Associated Proteins Are Present In Young Adult BrainsC. Kramer
Scientists have discovered that toxic, Alzheimer’s-associated proteins called beta-amyloids can build up in our brains far earlier in life than we originally thought — in our 20s!
What do beta-amyloids do? In brains affected by Alzheimer’s, beta-amyloids detach from the fatty membrane of nerve cells. Because they are sticky, they clump together. These clumps form plaques, and these plaques interfere with communication between cells and also trigger reactions that destroy nerve cells. The plaques work with another substance in the brain called tangles to break down the brain’s structure. This video animation gives a brief overview of the process.
For the study (published on March 2, 2015 in the scientific journal Brain), scientists at Northwestern University examined 50 brains, split up into three categories: cognitively normal people in an age range of 22 to 66; individuals aged 70 to 99 who didn’t have dementia; and people with Alzheimer’s aged 60 to 95.
They discovered that the beta-amyloids accrue inside neurons in the basal forebrain during early adulthood (and only in this area). They continue to accrue for the rest of our lives, growing in size and number.
“Discovering that amyloid begins to accumulate so early in life is unprecedented,” said lead investigator Changiz Geula. “This is very significant. We know that amyloid, when present for long periods of time, is bad for you.”
Since age is one of the biggest risks for Alzheimer’s, finding out exactly when the beta-amyloids start building up could be a major stepping stone to figuring out how to prevent Alzheimer’s. These proteins could be contributing to cell death in a number of ways, and with this new research in hand, scientists will investigate just how these amyloids are contributing to neuronal damage.
You can help. Help further Alzheimer’s research by donating to the Cure Alzheimer’s Fund, an organization dedicated to funding research with the highest probability of preventing, slowing, or reversing Alzheimer’s disease.