Memory loss is often the first sign of Alzheimer’s disease, followed by confusion and difficulty thinking. These symptoms reflect the typical pattern of worsening damage to brain tissues. Toxic clusters of proteins first concentrate in the temporal lobes of the brain — the memory area — before spreading to parts of the brain important for thinking and planning.
A study by researchers at Washington University School of Medicine in St. Louis yields clues to why certain parts of the brain are particularly vulnerable to Alzheimer’s damage. It comes down to the gene APOE, the greatest genetic risk factor for Alzheimer’s disease. The parts of the brain where APOE is most active are the areas that sustain the most damage, they found.
The findings, published Nov. 16 in Science Translational Medicine, help explain why symptoms of Alzheimer’s disease sometimes vary, and highlights an understudied aspect of Alzheimer’s disease that suggests yet-to-be discovered biological mechanisms may play an important role in the disease.
“There are some rare, what is lyrical dance class atypical forms of Alzheimer’s in which people first develop language or vision problems rather than memory problems,” said senior author Brian A. Gordon, PhD, an assistant professor of radiology at the School of Medicine’s Mallinckrodt Institute of Radiology. “When you scan their brains, you see damage to the language or the visual areas, and not so much to the memory areas. People with atypical Alzheimer’s are often screened out of research studies because it’s easier to study a group where everyone has the same set of symptoms. But this heterogeneity tells us that there are things we still don’t understand about how and why Alzheimer’s develops the way it does. There’s a reason why certain brain areas become damaged and not others, and we don’t know that reason yet. Every mystery we uncover with this disease pushes us closer to what we need to address it.”
Alzheimer’s disease begins with a brain protein known as amyloid beta. The protein starts building up into plaques two decades or more before people show the first signs of neurological problems. After years of amyloid accumulation, tangles of tau — another brain protein — begin to form. Soon after, tissues in the affected areas begin to wither and die, and cognitive decline sets in.
To understand why Alzheimer’s brain damage occurs where it does, Gordon and colleagues — including first author Aylin Dincer, a technician in Gordon’s lab — studied 350 people who volunteer for memory and aging studies through the School of Medicine’s Charles F. and Joanne Knight Alzheimer Disease Research Center. The participants underwent brain scans so the researchers could measure the amount and location of amyloid plaques and tau tangles, and the volumes of various brain areas.
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