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Article type: Research Article
Authors: Perry, TracyAnn; * | Greig, Nigel H.
Affiliations: Laboratory of Neuroscience, Section of Drug Design & Development, Gerontology Research Center, National Institute on Aging, National Institutes of Health, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
Correspondence: [*] Corresponding author. Tel.: +1 410 558 8104; Fax: +1 410 558 8323; E-mail: perryt@grc.nia.nih.gov.
Abstract: Glucagon-like peptide-1 (7-36)-amide (GLP-1) is an insulinotropic hormone, secreted from the enteroendocrine L cells of the intestinal tract in response to nutrient ingestion. It enhances pancreatic islet β-cell proliferation and glucose-dependent insulin secretion, and lowers blood glucose in patients with type 2 diabetes mellitus. GLP-1 receptors, which are coupled to the cyclic AMP second messenger pathway, are expressed throughout the brains of rodents and humans. The chemoarchitecture of receptor distribution in the brain correlates well with a central role for GLP-1 in the regulation of food intake and response to aversive stress. We have recently reported that GLP-1 and several longer acting analogs that bind at the GLP-1 receptor, possess neurotrophic properties, and offer protection against glutamate-induced apoptosis and oxidative injury in cultured neuronal cells. Furthermore, GLP-1 can modify processing of the amyloid β- protein precursor in cell culture and dose-dependently reduces amyloid β-peptide levels in the brain in vivo. As such, this review discusses the known role of GLP-1 within the central nervous system, and considers the potential of GLP-1 and analogs as novel therapeutic targets for intervention in Alzheimer's disease (AD) and potentially other central and peripheral neurodegenerative conditions.
DOI: 10.3233/JAD-2002-4605
Journal: Journal of Alzheimer's Disease, vol. 4, no. 6, pp. 487-496, 2002
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