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Exenatide exerts cognitive effects by modulating the BDNF-TrkB neurotrophic axis in adult mice.

Abstract：

:Modulation of insulin-dependent signaling is emerging as a valuable therapeutic tool to target neurodegeneration. In the brain, the activation of insulin receptors promotes cell growth, neuronal repair, and protection. Altered brain insulin signaling participates in the cognitive decline seen in Alzheimer's disease patients and the aging brain. Glucagon-like peptide-1 (GLP-1) regulates insulin secretion and, along with GLP-1 analogues, enhances neurotrophic signaling and counteracts cognitive deficits in preclinical models of neurodegeneration. Moreover, recent evidence indicates that GLP-1 modulates the activity of the brain-derived neurotrophic factor (BDNF). In this study, in adult wild-type mice, here employed as a model of mid-life brain aging, we evaluated the effects of a 2-month treatment with exenatide, a GLP-1 analogue. We found that exenatide promotes the enhancement of long-term memory performances. Biochemical and imaging analyses show that the drug promotes the activation of the BDNF-TrkB neurotrophic axis and inhibits apoptosis by decreasing p75NTR-mediated signaling. The study provides preclinical evidence for the use of exenatide to delay age-dependent cognitive decline.

journal_name

Neurobiol Aging

journal_title

Neurobiology of aging

authors

Bomba M,Granzotto A,Castelli V,Massetti N,Silvestri E,Canzoniero LMT,Cimini A,Sensi SL

doi

10.1016/j.neurobiolaging.2017.12.009

subject

Has Abstract

pub_date

2018-04-01 00:00:00

pages

33-43

eissn

0197-4580

issn

1558-1497

pii

S0197-4580(17)30404-9

journal_volume

64

pub_type

杂志文章

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