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Autophagy and neurodegeneration

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If you have a question about this talk, please contact Catherine Xu.

Intracellular protein aggregation is a feature of many late-onset neurodegenerative diseases, including Parkinson’s disease, tauopathies, and polyglutamine expansion diseases (like Huntington’s disease (HD)). Many of these mutant proteins, like that causing HD, cause disease via toxic gain-of-function mechanisms. Therefore, the factors regulating their clearance are crucial for understanding disease pathogenesis and for developing rational therapeutic strategies. We showed that the autophagy inducer, rapamycin, reduced the levels of mutant huntingtin and attenuated its toxicity in cells, and in Drosophila, zebrafish and mouse HD models. We have extended the range of intracellular proteinopathy substrates that are cleared by autophagy to other related neurodegenerative disease targets, like alpha-synuclein in Parkinson’s disease and tau in various dementias. While autophagy induction is protective in models of various neuro-degenerative diseases, many of these diseases are associated with compromised autophagy. I will discuss two of our studies describing how autophagy can be regulated. The first will consider how the amino acid leucine regulates autophagy via mTORC1. The second will describe our drug repurposing efforts to identify compounds already used in humans for other indications that may be suitable as autophagy inducers in the brain.

This talk is part of the Biophysical Seminars series.

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