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SUMMARY:Autophagy\, a guardian against neurodegeneration - Prof David Rubi
 nsztein
DTSTART:20231023T170000Z
DTEND:20231023T183000Z
UID:TALK205486@talks.cam.ac.uk
CONTACT:Drishtant Chakraborty
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\nWe showed that autophagy 
 induction reduces the levels of mutant huntingtin and attenuated its toxic
 ity in cells\, and in Drosophila\, zebrafish and mouse HD models. We have 
 extended the range of intracellular proteinopathy substrates that are clea
 red by autophagy to other related neurodegenerative disease targets\, like
  alpha-synuclein in Parkinson’s disease and tau in various dementias and
  Alzheimer’s disease. I will describe how autophagy is compromised in ce
 rtain neurodegenerative diseases and focus on recent data suggesting that 
 microglial-derived chemokines can compromise neuronal autophagy by activat
 ing CCR5 signalling. I will then consider how autophagy induction may be a
  powerful therapeutic approach for some of these conditions and describe d
 ifferent potential strategies and targets. \n
LOCATION:Pfizer Lecture Theatre\,  Department of Chemistry\, Lensfield Roa
 d
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