"Alzheimer's disease is widely believed to be caused by accumulating amyloid plaques in the brain, which trigger cascading effects that cause damage. But efforts to reduce amyloid plaques haven't reversed cognitive decline, causing some to wonder whether something else is going on."
"APOE4 plays a role in lipid transport in the brain but is worse at the task than APOE3. The result is lipids accumulating inside of brain cells and disruption of nerve cells' fatty myelin coating, which could affect how nerve signals move through the brain."
"When Akay's lab discovered that inhibiting a molecule called GSK3 beta reduced lipid accumulation inside of brain cells and improved myelination, they started TAC Therapeutics to develop the idea further."
Recent research challenges the traditional amyloid plaque hypothesis of Alzheimer's disease, as approved drugs reducing amyloid only slow cognitive decline without reversing it. Scientists are investigating alternative mechanisms, particularly fat metabolism disruptions in the brain. The APOE4 gene mutation impairs lipid transport compared to APOE3, causing lipids to accumulate inside brain cells and disrupting myelin coating around nerve cells, potentially affecting neural signal transmission. Researchers discovered that inhibiting GSK3 beta reduces lipid accumulation and improves myelination, leading to the development of new therapeutic approaches. Early results show promise, though substantial research remains necessary.
Read at Harvard Gazette
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