Metabolic and neurodegenerative disorders have a growing prevalence in Western countries. Available epidemiologic and neurobiological evidences support the existence of a pathophysiological link between these conditions. Glucagon-like peptide 1 (GLP-1), whose activity is reduced in insulin resistance, has been implicated in central nervous system function, including cognition, synaptic plasticity, and neurogenesis. We review the experimental researches suggesting that GLP-1 dysfunction might be a mediating factor between Type 2 diabetes mellitus (T2DM) and neurodegeneration. Drug treatments enhancing GLP-1 activity hold out hope for treatment and prevention of Alzheimer's disease (AD) and cognitive decline.

Glucagon-Like Peptide-1, Diabetes, and Cognitive Decline: Possible Pathophysiological Links and Therapeutic Opportunities / E.Mossello; E.Ballini; M.Boncinelli; M.Monami; G.Lonetto; AM.Mello; F.Tarantini; S.Baldasseroni; E.Mannucci; N.Marchionni. - In: EXPERIMENTAL DIABETES RESEARCH. - ISSN 1687-5214. - STAMPA. - 2011:(2011), pp. 0-0. [10.1155/2011/281674]

Glucagon-Like Peptide-1, Diabetes, and Cognitive Decline: Possible Pathophysiological Links and Therapeutic Opportunities

MOSSELLO, ENRICO;BALLINI, ELENA;BONCINELLI, MARTA;MONAMI, MATTEO;LONETTO, GIUSEPPE;MELLO, ANNAMARIA;TARANTINI, FRANCESCA;BALDASSERONI, SAMUELE;MANNUCCI, EDOARDO;MARCHIONNI, NICCOLO'
2011

Abstract

Metabolic and neurodegenerative disorders have a growing prevalence in Western countries. Available epidemiologic and neurobiological evidences support the existence of a pathophysiological link between these conditions. Glucagon-like peptide 1 (GLP-1), whose activity is reduced in insulin resistance, has been implicated in central nervous system function, including cognition, synaptic plasticity, and neurogenesis. We review the experimental researches suggesting that GLP-1 dysfunction might be a mediating factor between Type 2 diabetes mellitus (T2DM) and neurodegeneration. Drug treatments enhancing GLP-1 activity hold out hope for treatment and prevention of Alzheimer's disease (AD) and cognitive decline.
2011
2011
0
0
E.Mossello; E.Ballini; M.Boncinelli; M.Monami; G.Lonetto; AM.Mello; F.Tarantini; S.Baldasseroni; E.Mannucci; N.Marchionni
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Utilizza questo identificatore per citare o creare un link a questa risorsa: https://hdl.handle.net/2158/606314
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