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Scientists have revealed why certain parts of the brain are particularly vulnerable to damage from Alzheimer’s disease

Scientists have revealed why certain parts of the brain are particularly vulnerable to damage from Alzheimer’s disease. It is the APOE gene, the biggest genetic risk factor for the disease. According to researchers at the University of Washington, the parts of the brain where APOE is most active are the areas most damaged. Everyone carries some version of the APOE gene, but people who carry the APOE4 variant are up to 12 times more likely to develop Alzheimer’s than the general population, and at a younger age, they said.

The study’s findings, published in the journal Science Translational Medicine, help explain why Alzheimer’s disease symptoms sometimes vary and highlight an understudied aspect of Alzheimer’s disease that suggests as yet undiscovered biological mechanisms may play an important role in the disease. disease. Typical patterns of worsening brain tissue damage often begin with memory loss, followed by confusion and difficulty thinking. Toxic clumps of protein first concentrate in the memory area before spreading to parts of the brain important for thinking and planning.

However, as lead study author Brian A. Gordon said, there are some rare and atypical forms of Alzheimer’s disease in which people first develop language or vision problems rather than memory problems. “When you scan their brains, you see damage to language or visual areas and not so much memory areas. People with atypical Alzheimer’s disease are often left out of research studies because it’s easier to study a group where they all have the same group.” 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 some areas of the brain get damaged and others don’t, and we don’t know that reason yet.” Gordon said.

Alzheimer’s disease starts with a brain protein known as amyloid beta. The protein begins to accumulate in plaques two decades or more before people show the first signs of neurological problems. After years of amyloid build-up, tangles of tau, another brain protein, begin to form. Soon after, the tissues in the affected areas begin to wither and die, and cognitive function declines.

To understand why Alzheimer’s brain damage occurs where it does, Gordon and his colleagues studied 350 people who volunteered for memory and aging studies through the Charles F. and Joanne Knight Alzheimer’s Disease Research Center at the School of Medicine. The participants underwent brain scans so the researchers could measure the amount and location of amyloid plaques and tau clumps and the volumes of different brain regions, the study said.

The researchers compared the patterns of protein clumps and tissue damage in the volunteers with the gene expression patterns of APOE and other genes associated with Alzheimer’s disease, as shown in the Allen Human Brain Atlas, a detailed map of gene expression in the human brain compiled by the Allen Institute for Brain Sciences. “There was a close match between where you see high APOE expression and where you see tau tangles and tissue damage,” Gordon said.

“And not just APOE. If you look at, say, the top 20 genes associated with Alzheimer’s disease, they’re all expressed in the temporal lobes in similar patterns. There’s something fundamentally different about these regions that makes them vulnerable to Alzheimer’s brain damage, and that difference it’s probably baked in from birth and influenced by a person’s genetics.”

Alzheimer’s researchers have long known that APOE4 increases the accumulation of amyloid beta in human brains. By studying mice that develop tau tangles but not amyloid plaques, David Holtzman and colleagues showed that APOE4 also increases damage caused by tau, even in the absence of amyloid. To assess the effect of the high-risk APOE variant on tau-related brain damage in humans, the researchers classified each participant as carrying the high-risk variant or not and analyzed protein clusters and atrophy in their brains.

“APOE4 carriers are more likely to start accumulating amyloid, which puts them on the path to Alzheimer’s disease,” Gordon said. “Then for the same amount of amyloid, they get more tau tangles, which leads to more atrophy. It’s a double whammy in the brain.” Atrophy refers to weakening or degeneration, especially due to lack of use. In future work, Gordon and colleagues plan to examine how patterns of gene expression relate to patterns of tau damage in people with atypical Alzheimer’s disease. “When we see someone with vision problems, is there a specific genetic signature that corresponds to the areas that are damaged in the brain? We want to know why some people have these altered patterns and what that means, how Alzheimer’s develops and how it can be treated,” Gordon said.

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