Cargando…

Myelin injury induces axonal transport impairment but not AD-like pathology in the hippocampus of cuprizone-fed mice

Both multiple sclerosis (MS) and Alzheimer's disease (AD) are progressive neurological disorders with myelin injury and memory impairment. However, whether myelin impairment could cause AD-like neurological pathology remains unclear. To explore neurological pathology following myelin injury, we...

Descripción completa

Detalles Bibliográficos
Autores principales: Sun, Junjun, Zhou, Hong, Bai, Feng, Ren, Qingguo, Zhang, Zhijun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5058659/
https://www.ncbi.nlm.nih.gov/pubmed/27129150
http://dx.doi.org/10.18632/oncotarget.8981
_version_ 1782459275829837824
author Sun, Junjun
Zhou, Hong
Bai, Feng
Ren, Qingguo
Zhang, Zhijun
author_facet Sun, Junjun
Zhou, Hong
Bai, Feng
Ren, Qingguo
Zhang, Zhijun
author_sort Sun, Junjun
collection PubMed
description Both multiple sclerosis (MS) and Alzheimer's disease (AD) are progressive neurological disorders with myelin injury and memory impairment. However, whether myelin impairment could cause AD-like neurological pathology remains unclear. To explore neurological pathology following myelin injury, we assessed cognitive function, the expression of myelin proteins, axonal transport-associated proteins, axonal structural proteins, synapse-associated proteins, tau and beta amyloid and the status of neurons, using the cuprizone mouse model of demyelination. We found the mild impairment of learning ability in cuprizone-fed mice and the decreased expression of myelin basic protein (MBP) in the hippocampus. And anti-LINGO-1 improved learning ability and partly restored MBP level. Furthermore, we also found kinesin light chain (KLC), neurofilament light chain (NFL) and neurofilament heavy chain (NF200) were declined in demyelinated hippocampus, which could be partly improved by treatment with anti-LINGO-1. However, we did not observe the increased expression of beta amyloid, hyperphosphorylation of tau and loss of neurons in demyelinated hippocampus. Our results suggest that demyelination might lead to the impairment of neuronal transport, but not cause increased level of hyperphosphorylated tau and beta amyloid. Our research demonstrates remyelination might be an effective pathway to recover the function of neuronal axons and cognition in MS.
format Online
Article
Text
id pubmed-5058659
institution National Center for Biotechnology Information
language English
publishDate 2016
publisher Impact Journals LLC
record_format MEDLINE/PubMed
spelling pubmed-50586592016-10-15 Myelin injury induces axonal transport impairment but not AD-like pathology in the hippocampus of cuprizone-fed mice Sun, Junjun Zhou, Hong Bai, Feng Ren, Qingguo Zhang, Zhijun Oncotarget Research Paper: Gerotarget (Focus on Aging) Both multiple sclerosis (MS) and Alzheimer's disease (AD) are progressive neurological disorders with myelin injury and memory impairment. However, whether myelin impairment could cause AD-like neurological pathology remains unclear. To explore neurological pathology following myelin injury, we assessed cognitive function, the expression of myelin proteins, axonal transport-associated proteins, axonal structural proteins, synapse-associated proteins, tau and beta amyloid and the status of neurons, using the cuprizone mouse model of demyelination. We found the mild impairment of learning ability in cuprizone-fed mice and the decreased expression of myelin basic protein (MBP) in the hippocampus. And anti-LINGO-1 improved learning ability and partly restored MBP level. Furthermore, we also found kinesin light chain (KLC), neurofilament light chain (NFL) and neurofilament heavy chain (NF200) were declined in demyelinated hippocampus, which could be partly improved by treatment with anti-LINGO-1. However, we did not observe the increased expression of beta amyloid, hyperphosphorylation of tau and loss of neurons in demyelinated hippocampus. Our results suggest that demyelination might lead to the impairment of neuronal transport, but not cause increased level of hyperphosphorylated tau and beta amyloid. Our research demonstrates remyelination might be an effective pathway to recover the function of neuronal axons and cognition in MS. Impact Journals LLC 2016-04-25 /pmc/articles/PMC5058659/ /pubmed/27129150 http://dx.doi.org/10.18632/oncotarget.8981 Text en Copyright: © 2016 Sun et al. http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper: Gerotarget (Focus on Aging)
Sun, Junjun
Zhou, Hong
Bai, Feng
Ren, Qingguo
Zhang, Zhijun
Myelin injury induces axonal transport impairment but not AD-like pathology in the hippocampus of cuprizone-fed mice
title Myelin injury induces axonal transport impairment but not AD-like pathology in the hippocampus of cuprizone-fed mice
title_full Myelin injury induces axonal transport impairment but not AD-like pathology in the hippocampus of cuprizone-fed mice
title_fullStr Myelin injury induces axonal transport impairment but not AD-like pathology in the hippocampus of cuprizone-fed mice
title_full_unstemmed Myelin injury induces axonal transport impairment but not AD-like pathology in the hippocampus of cuprizone-fed mice
title_short Myelin injury induces axonal transport impairment but not AD-like pathology in the hippocampus of cuprizone-fed mice
title_sort myelin injury induces axonal transport impairment but not ad-like pathology in the hippocampus of cuprizone-fed mice
topic Research Paper: Gerotarget (Focus on Aging)
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5058659/
https://www.ncbi.nlm.nih.gov/pubmed/27129150
http://dx.doi.org/10.18632/oncotarget.8981
work_keys_str_mv AT sunjunjun myelininjuryinducesaxonaltransportimpairmentbutnotadlikepathologyinthehippocampusofcuprizonefedmice
AT zhouhong myelininjuryinducesaxonaltransportimpairmentbutnotadlikepathologyinthehippocampusofcuprizonefedmice
AT baifeng myelininjuryinducesaxonaltransportimpairmentbutnotadlikepathologyinthehippocampusofcuprizonefedmice
AT renqingguo myelininjuryinducesaxonaltransportimpairmentbutnotadlikepathologyinthehippocampusofcuprizonefedmice
AT zhangzhijun myelininjuryinducesaxonaltransportimpairmentbutnotadlikepathologyinthehippocampusofcuprizonefedmice