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SUMMARY:Special LMNN Seminar // Translation regulation in Neurodegenerativ
 e diseases: What we know about elongation factor-2 kinase (eEF2K) in Alzhe
 imer’s disease.
DTSTART:20170523T140000
DTEND:20170523T150000
DTSTAMP:20260427T203631Z
UID:9d02fd9ec6cbb808c6da27c51d866e7e0e4b5f99021967d29c06be89
CATEGORIES:Conferences - Seminars
DESCRIPTION:Asad Jan University of British Columbia\,\nBC Cancer Research 
 Centre\nVancouver\, Canada\nmRNA translation and protein synthesis at syna
 pses are tightly coupled to synaptic activity\, and play an essential role
  in the long lasting forms of synaptic plasticity. A key molecule regulati
 ng dendritic mRNA translation is the calcium/Calmodulin dependent elongati
 on factor-2 kinase (eEF2K)\, which is activated in response to glutamaterg
 ic neurotransmission. During this presentation\, I will describe some rece
 nt literature\, including our own published data\, on the relevance of eEF
 2K to Alzheimer’s disease neuropathology. We have found that eEF2K inhib
 ition blocks the toxicity of amyloid-β (Aβ) oligomers in neuronal cultur
 es by activating Nuclear factor erythroid-derived 2-like 2 (NRF2)\, a mast
 er regulator of antioxidant response. Furthermore\, in the transgenic APP/
 PS1 mice of cerebral Aβ amyloidosis\, eEF2K activity is particularly incr
 eased in the granule cell layer (GCL) neurons of the hippocampal dentate g
 yrus\, implicating eEF2K activity in the adult neurogenesis. Our recent da
 ta indicate that aberrant eEF2K activity is also relevant to neuropatholog
 y of Parkinson disease and motor neurone disease. Various experimental app
 roaches\, including genome editing by CRISPR/Cas9\, to target eEF2K in pre
 -clinical rodent models will also be discussed.
LOCATION:AI  1153
STATUS:CONFIRMED
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