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SUMMARY:A Drosophila Model for the role of ApoE in Alzheimer’s Disease. 
 - Paul Hopkins\, King's College London
DTSTART:20110705T100000Z
DTEND:20110705T110000Z
UID:TALK31746@talks.cam.ac.uk
CONTACT:Dr Douglas Griffith
DESCRIPTION:The lifetime risk of developing Alzheimer’s disease (AD) var
 ies from under 1% to over 60% according to apolipoprotein E (apoE) genotyp
 e\; apoE is therefore the most significant common genetic risk factor for 
 late onset AD\, with the apoE4 isoform leading to an earlier onset of AD c
 ompared to the apoE3 isoform\, and the apoE2 isoform being protective.\n \
 nEarly- and late-onset AD are pathologically similar conditions characteri
 sed by accumulation of the b-amyloid peptide as plaques.  This peptide is 
 generated from the amyloid precursor protein (APP) by presenilin.  Mutatio
 ns in either presenilin or APP lead to early onset AD.\n \nWe have identif
 ied a previously unstudied neuronal protein that has an\nisoform-specific 
 binding to apoE3 and apoE4\, forms a complex with APP and has a differenti
 al cellular interaction with normal versus pathogenic forms of APP.  This 
 interaction increases the production of b-amyloid [in press].\n  \nHere we
  present a model for the function of the Drosophila orthologue of this pro
 tein\, that we call dementin.  We show that dementin is necessary for norm
 al brain development\, and interacts both with human APP and with the Dros
 ophila APP-like protein.  Further\, we show that neuronal disruption of de
 mentin leads to neurodegeneration.\n \nOur findings may therefore form a m
 olecular link between established risk factors for early and late onset AD
 .\n
LOCATION:Part II Room\, Department of Genetics\,
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