Alzheimer's disease affects more than 6 million people in the United States, and there are very few FDA-approved treatments that can slow the progression of the disease.
The findings suggest that an interplay of genetic and epigenetic changes feed on each other to drive the pathological manifestations of the disease. In the study led by Mathys, the researchers also compared gene expression patterns in people who showed cognitive impairments and those who did not, including some who remained sharp despite having some degree of amyloid buildup in the brain, a phenomenon known as cognitive resilience. That analysis revealed that cognitively resilient people had larger populations of two subsets of inhibitory neurons in the prefrontal cortex.
This study also revealed that every type of cell in the brain undergoes a phenomenon known as epigenomic erosion as Alzheimer's disease progresses, meaning that the cells' normal pattern of accessible genomic sites is lost, which contributes to loss of cell identity.paper, led by MIT graduate student Na Sun and research scientist Matheus Victor, the researchers focused primarily on microglia, which make up 5 to 10 percent of the cells in the brain.
This fourth study found that as more DNA damage accumulates in neurons, it becomes more difficult for them to repair the damage, leading to genome rearrangements and 3D folding defects.
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