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Modulating rapamycin target protein promotes autophagy, lowering toxic Huntingtin protein

Recent failed clinical trials of a drug designed to clear the mutant Huntingtin protein that causes Huntington s disease (HD) heightens the need for new approaches for the devastating, incurable, progressive neurodegenerative genetic disorder. Scientists at the Buck Institute have found that the targeting the protein called FK506-binding protein 51 or FKBP51 promotes the clearing of those toxic proteins via autophagy, a natural process whereby cells recycle damaged proteins and mitochondria and use them for nutrition.

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