Research shows depletion of mitochondria in neuron axons leads to protein build-up, a key factor in neurodegenerative diseases, offering a new target for treatment. Credit: SciTechDaily.com. They used fruit flies to show that depletion of mitochondria in axons can directly lead to protein accumulation. At the same time, significantly high amounts of a protein called eIF2β were found. Restoring the levels to normal led to a recovery in protein recycling.
They focused on the presence of mitochondria in axons, the long tendril-like appendages that stretch out of neurons and form the necessary connections that allow signals to be transmitted inside our brains. It is known that the levels of mitochondria in axons can drop with age, and during the progress of neurodegenerative diseases.Now, the team has discovered that the depletion of mitochondria in axons has a direct bearing on protein build-up.
Through proteomic analysis, they were able to identify a significant upregulation in eIF2β, a key subunit of the eIF2 protein complex responsible for the initiation of protein production . The eIF2α subunit was also found to be chemically modified. Both of these issues hamper the healthy action of eIF2.
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