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SUMMARY:B-arrestin modulation of GPCR function in Alzheimer's Disease - D 
 Amantha Thathiah\, Department of Human Molecular Genetics\, Catholic Unive
 rsity of Leuven (KU Leuven)\, Belgium
DTSTART:20140122T161500Z
DTEND:20140122T171500Z
UID:TALK50443@talks.cam.ac.uk
CONTACT:Dr Michael Hastings
DESCRIPTION:G protein-coupled receptors (GPCRs) are involved in numerous n
 eurotransmitter systems which are disrupted in the brains of Alzheimer’s
  disease (AD) patients. GPCRs are also associated with multiple stages of 
 β-amyloid precursor protein (APP) proteolysis\, including modulation of t
 he α-\, β-\, and γ-secretase processing of APP and regulation of Aβdeg
 radation and Aβ-mediated neurotoxicity\, indicating an intimate associati
 on between GPCRs and the molecular pathways involved in AD. We recently id
 entified GPR3\, a constitutively active orphan GPCR\, as an /in vitro /and
  /in vivo /modulator of Abgeneration and determined that GPR3 levels are e
 levated in a subset of AD patients.To further address the mechanism of act
 ion of the GPR3-mediated effect on Abgeneration\, we then focused on a sma
 ll family of multifunctional GPCR regulatory proteins known as the β-arre
 stins\, which play an almost universal role in facilitating traditional GP
 CR desensitization but which are also capable of initiating distinct signa
 ls in their own right\, conveying receptor subtype-specific signaling even
 ts. These signals are often both spatially and temporally distinct\, and r
 esult in unique cellular and physiological or pathophysiological consequen
 ces.As mediators of GPCR desensitization\, trafficking and cell signaling\
 , the β-arrestins provide a putative basis to understand GPCR dysfunction
  in AD. In this talk\, I will address the involvement of GPR3 in the patho
 genesis of AD and discuss the role of b-arrestin 2 in modulation of γ-sec
 retase activity and Abgeneration in AD.\nHost: Michael Hastings\n
LOCATION:Max Perutz Lecture Theatre\, MRC Laboratory of Molecular Biology
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