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SUMMARY:BMI Seminar // Synaptotoxicity in Alzheimer’s disease: a new the
 rapeutic target
DTSTART:20171220T121500
DTEND:20171220T131500
DTSTAMP:20260506T071615Z
UID:84705b026e547c09ab064ad1aaf9f72d084cbb5f75d491370e696bc5
CATEGORIES:Conferences - Seminars
DESCRIPTION:Alain Buisson\, Neuropathologies and Synaptic Dysfunctions\, N
 eurosciences Institute\, Grenoble\, France\nAlzheimer’s disease (AD) is 
 a neurodegenerative disease that affects memory. A large body of evidence 
 has implicated Amyloid β1-42 protein (Aβ) and other cleavage products of
  the amyloid precursor protein (APP) as central to synaptic plasticity dis
 ruption. Similarly fibrillar deposits of phosphorylated tau are a characte
 ristic feature of several neurodegenerative diseases including AD.  Tau i
 s a microtubule-associated protein well known for its stabilization of mic
 rotubules in axons. Recently\, it has emerged that tau participates in syn
 aptic function as part of the molecular pathway leading to Aβ-driven syna
 ptotoxicity in the context of AD. In this presentation\, I will describe t
 he implication of tau in the profound functional synaptic modification ass
 ociated with synaptic plasticity and how AD mimicking conditions induce a 
 mislocalization of tau into the post synaptic sites of excitatory synapses
 . We focused on 4 isoforms of human neuronal APP: APP695 Wild-type (APPwt)
  and APP695 Swedish (K670N/M671L) (APPswe) that both increase Aβ producti
 on\; APP695 Osaka (E693Δ) (APPosa) which induces an intracellular accumul
 ation of Aβ\; and APP695 Icelandic (A673T) (APPice) a mutant that decreas
 es Aβ production and allegedly protects against AD. I will further descri
 be the consequence of the expression of different pathologic mutants of AP
 P\, which promote contrasting profile of productions of Aβ\, in order to 
 define their impact on the morphology and function of excitatory synapses.
  Together\, these results will highlight the central role of excitatory sy
 napses dysfunctions in the physiopathology of AD.\n \n 
LOCATION:SV 1717 https://plan.epfl.ch/?room==SV%201717
STATUS:CONFIRMED
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