The scientific community has long believed that beta-amyloid, a protein that can clump together and form sticky plaques in the brain, is the first sign of Alzheimer’s disease.
Beta-amyloid then leads to other brain changes including neurodegeneration and eventually to thinking and memory problems.
But in a new study, researchers suggest that subtle thinking and memory differences may come before, or happen alongside, the development of amyloid plaques that can be detected in the brain.
The research was conducted by a team at the VA San Diego Healthcare System.
The study involved 747 people with an average age of 72.
The researchers gave participants neuropsychological tests at the beginning of the study and measured their total scores and also their process scores to determine if they had subtle thinking and memory difficulties.
They divided participants into three groups: 305 people with normal thinking and memory skills; 153 with subtle thinking and memory differences; and 289 people with mild cognitive impairment.
Participants had brain scans at the start of the study to determine levels of amyloid plaques in the brain, and then yearly scans for four years.
The researchers found people with subtle thinking and memory differences had a more rapid accumulation of amyloid compared to people with normal thinking and memory skills.
On a test that uses a dye to measure amyloid levels, where the average level was 1.16 for participants with subtle thinking and memory difficulties, amyloid levels in this group increased by .03 above and beyond the amyloid changes in those with normal thinking and memory skills over four years.
People with subtle differences also had faster thinning of the entorhinal cortex, a brain region that is impacted very early in Alzheimer’s disease.
On the other hand, while people with mild cognitive impairment had more amyloid in their brains at the beginning of the study, they did not have a faster accumulation of amyloid when compared to those with normal thinking and memory skills.
However, they did have faster thinning of the entorhinal cortex as well as brain shrinkage of the hippocampus.
The findings show that amyloid may not necessarily come first in the Alzheimer’s disease process.
Much of the research exploring possible treatments for Alzheimer’s disease has focused on targeting amyloid.
But based on these findings, perhaps that focus needs to shift to other possible targets.
Another biomarker of Alzheimer’s disease, a protein called tau, shows a consistent relationship with thinking and memory symptoms.
More research is needed to determine if tau is already present in the brain when subtle thinking and memory differences begin to appear.
One author of the study is Kelsey R. Thomas, Ph.D. at the VA San Diego Healthcare System in San Diego.
The study is published in Neurology.
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