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SUMMARY:Autophagy and neurodegeneration - Professor David Rubinsztein ( CI
 MR)
DTSTART:20191127T103000Z
DTEND:20191127T113000Z
UID:TALK135100@talks.cam.ac.uk
CONTACT:Catherine Xu
DESCRIPTION:Intracellular protein aggregation is a feature of many late-on
 set neurodegenerative diseases\, including Parkinson’s disease\, tauopat
 hies\, 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 fo
 r developing rational therapeutic strategies.\n     We showed that the aut
 ophagy inducer\, rapamycin\, reduced the levels of mutant huntingtin and a
 ttenuated its toxicity in cells\, and in _Drosophila_\, zebrafish and mous
 e HD models. We have extended the range of intracellular proteinopathy sub
 strates that are cleared by autophagy to other related neurodegenerative d
 isease targets\, like alpha-synuclein in Parkinson’s disease and tau in 
 various dementias. While autophagy induction is protective in models of va
 rious neuro-degenerative diseases\, many of these diseases are associated 
 with compromised autophagy. I will discuss two of our studies describing h
 ow 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. \n
LOCATION:Department of Chemistry\, Cambridge\, Todd Hamied Room
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