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SUMMARY:Keeping axons alive after injury: Inhibiting programmed axon death
  - Dr Stacey Gould\, Department of Clinical Neurosciences
DTSTART:20211110T170000Z
DTEND:20211110T180000Z
UID:TALK165727@talks.cam.ac.uk
CONTACT:Katharina Zuhlsdorff
DESCRIPTION:Activation of pro-degenerative protein SARM1 in response to di
 verse physical and disease-relevant injuries triggers programmed axon deat
 h. Original studies indicated substantially decreased levels of SARM1 were
  required for neuroprotection. However\, we demonstrate that lowering SARM
 1 levels by 50% in Sarm1 haploinsufficient mice delays axon degeneration i
 n vivo (after sciatic nerve transection)\,  in vitro (in response to diver
 se traumatic\, neurotoxic\, and genetic triggers)\, and partially prevents
  neurite outgrowth defects in mice lacking pro-survival factor NMNAT2. We 
 also demonstrate the capacity for Sarm1 antisense oligonucleotides to decr
 ease SARM1 levels by more than 50% which delays or prevents programmed axo
 n degeneration in vitro. Combining Sarm1 haploinsufficiency with antisense
  oligonucleotides further decreases SARM1 levels and prolongs protection a
 fter neurotoxic injuries. These data demonstrate that axon protection occu
 rs in a Sarm1 gene-dose responsive manner and that SARM1 lowering agents h
 ave therapeutic potential. Thus\, antisense oligonucleotide targeting of S
 arm1 is a promising therapeutic strategy against diverse triggers of axon 
 degeneration.\n\n
LOCATION:Zoom
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