B-arrestin modulation of GPCR function in Alzheimer's Disease

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• D Amantha Thathiah, Department of Human Molecular Genetics, Catholic University of Leuven (KU Leuven), Belgium
• Wednesday 22 January 2014, 16:15-17:15
• Max Perutz Lecture Theatre, MRC Laboratory of Molecular Biology.

If you have a question about this talk, please contact Dr Michael Hastings.

G protein-coupled receptors (GPCRs) are involved in numerous neurotransmitter systems which are disrupted in the brains of Alzheimer’s disease (AD) patients. GPC Rs are also associated with multiple stages of β-amyloid precursor protein (APP) proteolysis, including modulation of the α-, β-, and γ-secretase processing of APP and regulation of Aβdegradation and Aβ-mediated neurotoxicity, indicating an intimate association between GPC Rs and the molecular pathways involved in AD. We recently identified GPR3 , a constitutively active orphan GPCR , as an /in vitro /and /in vivo /modulator of Abgeneration and determined that GPR3 levels are elevated in a subset of AD patients.To further address the mechanism of action of the GPR3 -mediated effect on Abgeneration, we then focused on a small family of multifunctional GPCR regulatory proteins known as the β-arrestins, which play an almost universal role in facilitating traditional GPCR desensitization but which are also capable of initiating distinct signals in their own right, conveying receptor subtype-specific signaling events. These signals are often both spatially and temporally distinct, and result in unique cellular and physiological or pathophysiological consequences.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 pathogenesis of AD and discuss the role of b-arrestin 2 in modulation of γ-secretase activity and Abgeneration in AD. Host: Michael Hastings

This talk is part of the Cambridge Neuroscience Seminars series.

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