Department of Pharmacology
Pharmacology and Neuroscience Graduate Program
Seminar
ROLE OF WNT SIGNALING IN ALZHEIMER’S DIS...
Spring 2010-Seminar Flier
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Spring 2010-Seminar Flier

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Spring 2010-Seminar Flier

  1. 1. Department of Pharmacology Pharmacology and Neuroscience Graduate Program Seminar ROLE OF WNT SIGNALING IN ALZHEIMER’S DISEASE PATHOGENESIS Presented by: Nisha Rizvi Tuesday, April 20, 2010 – 3:00 p.m. Med-Micro SCLF II Conference Room 825 North Rutledge Springfield, Illinois Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by abnormal deposition of extracellular β-amyloid plaques and intracellular hyperphosphorylated tau tangles. Many theories related to the pathogenesis of AD have been proposed and are being studied extensively. One of them suggests that a dysfunctional Wnt signaling pathway, at least in part, may be associated with altered transcriptional regulation of target genes leading to metabolic defects and activation of apoptotic signals for progressive and selective death of specific neuronal cell populations. Wnt pathway is a critical mediator of intercellular signaling events through highly conserved family of secreted proteins involved in multiple developmental events during embryogenesis and adult tissue homeostasis. It is extensively being studied for its involvement in the pathogenesis of a number of diseases like diabetes, cancer, schizophrenia and Alzheimer’s disease. In the mature nervous system, expression of Wnt signaling suggests its role in maintenance of synaptic structure, function and plasticity. It modulates both pre- and postsynaptic protein clustering important for neurite growth and establishment of new functional synapses which may contribute to long term potentiation (LTP). Neuronal exposure to Aβ induces alteration in expression and/or activity of various canonical and non-canonical Wnt proteins such as the frizzled (Fz)/ low density lipoprotein receptor-related protein (LRP) complex, disheveled (Dsh), glycogen synthase kinase-3β (GSK-3β), and β-catenin ultimately leading to neurodegeneration. Also, recent studies report that Wnt signaling interacts with peroxisome proliferator-activated receptor γ (PPARγ) and muscarinic acetylcholine receptor (mAChR) pathways together eliciting neuroprotection. Thus, there is growing evidence that Wnt signaling is a putative target for Aβ-dependent synaptotoxicity and its activation by Wnt ligands, PPARγ or M1 mAChR agonists could serve as a potential therapeutic strategy in Alzheimer’s disease.

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