The study discovered that as Alzheimer's disease progresses, brain levels of enzymes that regulate DNA-folding decrease. Researchers from the University of Pittsburgh, McGill University, and Harvard University found that, in contrast to earlier research, the levels of brain enzymes that control DNA
These dogma-challenging findings show that decreased levels of Histone Deacetylase I , one of the enzymes that control how DNA is packaged inside the cell’s nucleus, are associated with the negative effects of misfolded beta-amyloid and tau proteins and Alzheimer’s disease-associated cognitive decline. These results were verified across two independent cohorts of live patients with Alzheimer’s disease as well as on post-mortem brain tissues.
“Approximately one-third of elders who have brain amyloid pathology do not develop Alzheimer’s disease,” said lead author Tharick Pascoal M.D. He is also an assistant professor of psychiatry and neurology at Pitt’s School of Medicine. He continues, “Now we have evidence of another factor that dictates whether or not the disease will progress further, and it is related to how the brain environment can affect the expression of our genes.
One of these processes is known as epigenetic histone modification. A cell may adjust the efficiency with which genetic information is translated into templates for new proteins by modifying how DNA is folded within its nucleus—whether it is tightly wrapped around protein barrels called histones or hung in looser threads. This permits the cell to swiftly and reversibly modify the way our genes operate and react to changes in the environment without changing the DNA sequence itself.
Earlier studies on post-mortem brain samples reported that levels of HDACs in the brains of patients with Alzheimer’s increase as the disease progresses. High levels of HDACs were thought to restrict the brain’s ability to produce new functional proteins that make up critical cell components and, therefore, contribute to memory loss and cognitive decline.
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