4.5 Article

REGULAR EXERCISE PROMOTES MEMORY FUNCTION AND ENHANCES HIPPOCAMPAL NEUROPLASTICITY IN EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS MICE

Journal

NEUROSCIENCE
Volume 346, Issue -, Pages 173-181

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2017.01.016

Keywords

multiple sclerosis; exercise; memory; BDNF

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Funding

  1. Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Science, ICT & Future Planning [NRF-2014R1A1A3052861]
  2. National Research Foundation of Korea [2014R1A1A3052861] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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Multiple sclerosis (MS) is a progressive condition affecting the central nervous system (CNS), and is characterized by the development of demyelinated lesions and plaques in the brain and spinal cord. Exercise is beneficial against dementia in elderly patients, so we investigated the effects of exercise on memory in relation to hippocampal demyelination and neuroplasticity in a mouse model of MS (experimental autoimmune encephalomyelitis [EAE]). Mice were randomly divided into three groups: Sham, EAE, and EAE and exercise (EAE + EX). EAE + EX mice exercised five times a week for 4 weeks, and all mice performed step-down avoidance tasks in order to verify memory ability. We analyzed changes in myelin basic protein (MBP), 2',3'-Cyclic nucleotide 3'-phosphodiesterase (CNPase), 5-bromo-2'-deoxyuridine (brdU), doublecortin (DCX), bcl-2, bax, TUNEL, caspase-3, and brain derived neurotrophic factor (BDNF) via immunoassay or histological staining. We found decreased memory ability in EAE mice, accompanied by impaired myelination, increased apoptosis and cell proliferation, and decreased BDNF in the hippocampus. The memory decline and changes in demyelination, apoptosis, BDNF, and cell proliferation were partially reversed in EAE + EX mice. Our findings suggest that in patients with MS, regular exercise may benefit cognitive function by rescuing some hippocampal cellular and molecular impairments. (C) 2017 IBRO. Published by Elsevier Ltd. All rights reserved.

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