Japanese researchers discover that mitochondria depletion in axons leads to protein accumulation in neurodegenerative diseases, and restoring eIF2β levels improves protein recycling.

Japanese researchers identify how abnormal protein build-up in neurons, a feature of neurodegenerative diseases like Alzheimer's, occurs. Depletion of mitochondria in axons was found to directly lead to protein accumulation, with high levels of eIF2β protein detected. Restoring eIF2β levels improved protein recycling, suggesting potential new treatments for neurodegenerative diseases.

April 20, 2024
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