Low field magnetic stimulation promotes myelin repair and cognitive recovery in chronic cuprizone mouse model

Background Multiple sclerosis (MS) is an inflammatory demyelinating disease featured with neuroinflammation, demyelination, and the loss of oligodendrocytes. Cognitive impairment and depression are common neuropsychiatric symptoms in MS that are poorly managed with the present interventions. Objecti...

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Veröffentlicht in:Clinical and experimental pharmacology & physiology 2021-08, Vol.48 (8), p.1090-1102
Hauptverfasser: Wang, Zitong, Baharani, Akanksha, Wei, Zelan, Truong, Davin, Bi, Xiaoying, Wang, Fei, Li, Xin‐Min, Verge, Valerie M. K., Zhang, Yanbo
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container_end_page 1102
container_issue 8
container_start_page 1090
container_title Clinical and experimental pharmacology & physiology
container_volume 48
creator Wang, Zitong
Baharani, Akanksha
Wei, Zelan
Truong, Davin
Bi, Xiaoying
Wang, Fei
Li, Xin‐Min
Verge, Valerie M. K.
Zhang, Yanbo
description Background Multiple sclerosis (MS) is an inflammatory demyelinating disease featured with neuroinflammation, demyelination, and the loss of oligodendrocytes. Cognitive impairment and depression are common neuropsychiatric symptoms in MS that are poorly managed with the present interventions. Objective This study aimed to investigate the effects of low field magnetic stimulation (LFMS), a novel non‐invasive neuromodulation technology, on cognitive impairment and depressive symptoms associated with MS using a mouse model of demyelination. Methods C57BL female mice were fed with a 0.2% cuprizone diet for 12 weeks to induce a chronic demyelinating model followed by 4 weeks of cuprizone withdrawal with either sham or LFMS treatment. Results Improved cognition and depression‐like behaviour and restored weight gain were observed in mice with LFMS treatment. Immunohistochemical and immunoblotting data showed enhanced myelin basic protein (MBP) and myelin oligodendrocyte glycoprotein expressions (MOG) in the prefrontal cortex of mice with LFMS treatment, supporting that myelin repair was promoted. LFMS also increased the protein expression of mature oligodendrocyte biomarker glutathione‐S‐transferase (GST‐π). In addition, expression of TGF‐β and associated receptors were elevated with LFMS treatment, implicating this pathway in the response. Conclusion Results from the present study revealed LFMS to have neuroprotective effects, suggesting that LFMS has potential therapeutic value for treating cognitive impairment and depression related to demyelination disorders. Low field magnetic stimulation (LFMS) is a non‐invasive brain stimulation device that improved cognition and depression‐like behaviour and promoted myelin repair and oligodendrocyte maturation in a chronic cuprizone intoxication animal model. The transforming growth factor‐beta signaling pathway may be activated due to LFMS. This study suggests that LFMS has therapeutic potential in demyelinating diseases and related cognitive impairment and depression.
doi_str_mv 10.1111/1440-1681.13490
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K. ; Zhang, Yanbo</creator><creatorcontrib>Wang, Zitong ; Baharani, Akanksha ; Wei, Zelan ; Truong, Davin ; Bi, Xiaoying ; Wang, Fei ; Li, Xin‐Min ; Verge, Valerie M. K. ; Zhang, Yanbo</creatorcontrib><description>Background Multiple sclerosis (MS) is an inflammatory demyelinating disease featured with neuroinflammation, demyelination, and the loss of oligodendrocytes. Cognitive impairment and depression are common neuropsychiatric symptoms in MS that are poorly managed with the present interventions. Objective This study aimed to investigate the effects of low field magnetic stimulation (LFMS), a novel non‐invasive neuromodulation technology, on cognitive impairment and depressive symptoms associated with MS using a mouse model of demyelination. Methods C57BL female mice were fed with a 0.2% cuprizone diet for 12 weeks to induce a chronic demyelinating model followed by 4 weeks of cuprizone withdrawal with either sham or LFMS treatment. Results Improved cognition and depression‐like behaviour and restored weight gain were observed in mice with LFMS treatment. Immunohistochemical and immunoblotting data showed enhanced myelin basic protein (MBP) and myelin oligodendrocyte glycoprotein expressions (MOG) in the prefrontal cortex of mice with LFMS treatment, supporting that myelin repair was promoted. LFMS also increased the protein expression of mature oligodendrocyte biomarker glutathione‐S‐transferase (GST‐π). In addition, expression of TGF‐β and associated receptors were elevated with LFMS treatment, implicating this pathway in the response. Conclusion Results from the present study revealed LFMS to have neuroprotective effects, suggesting that LFMS has potential therapeutic value for treating cognitive impairment and depression related to demyelination disorders. Low field magnetic stimulation (LFMS) is a non‐invasive brain stimulation device that improved cognition and depression‐like behaviour and promoted myelin repair and oligodendrocyte maturation in a chronic cuprizone intoxication animal model. The transforming growth factor‐beta signaling pathway may be activated due to LFMS. This study suggests that LFMS has therapeutic potential in demyelinating diseases and related cognitive impairment and depression.</description><identifier>ISSN: 0305-1870</identifier><identifier>ISSN: 1440-1681</identifier><identifier>EISSN: 1440-1681</identifier><identifier>DOI: 10.1111/1440-1681.13490</identifier><identifier>PMID: 33638234</identifier><language>eng</language><publisher>Australia: Wiley Subscription Services, Inc</publisher><subject>Animals ; Biomarkers ; Body weight gain ; Cognition ; Cognitive ability ; Cognitive Dysfunction - chemically induced ; Cognitive Dysfunction - metabolism ; Cognitive Dysfunction - therapy ; Cuprizone ; Demyelinating diseases ; Demyelinating Diseases - chemically induced ; Demyelinating Diseases - metabolism ; Demyelinating Diseases - therapy ; Demyelination ; Disease Models, Animal ; Female ; Glutathione ; Glycoproteins ; Immunoblotting ; Impairment ; LFMS ; Magnetic Field Therapy - methods ; Magnetic fields ; Mental depression ; Mice ; Mice, Inbred C57BL ; Multiple sclerosis ; Multiple Sclerosis - chemically induced ; Multiple Sclerosis - metabolism ; Multiple Sclerosis - therapy ; Myelin ; Myelin basic protein ; Myelin Sheath - metabolism ; Neuromodulation ; Neuroprotection ; Oligodendrocyte-myelin glycoprotein ; Oligodendrocytes ; Prefrontal cortex ; Proteins ; Recovery of Function ; remyelination ; Repair ; Signs and symptoms ; Stimulation</subject><ispartof>Clinical and experimental pharmacology &amp; physiology, 2021-08, Vol.48 (8), p.1090-1102</ispartof><rights>2021 John Wiley &amp; Sons Australia, Ltd</rights><rights>2021 John Wiley &amp; Sons Australia, Ltd.</rights><rights>Copyright © 2021 John Wiley &amp; Sons Australia, Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4370-307888be274fe7952586ed121c5a5fce620001db38a8857240472551ad8796f13</citedby><cites>FETCH-LOGICAL-c4370-307888be274fe7952586ed121c5a5fce620001db38a8857240472551ad8796f13</cites><orcidid>0000-0002-2421-157X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2F1440-1681.13490$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2F1440-1681.13490$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1416,27923,27924,45573,45574</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33638234$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Zitong</creatorcontrib><creatorcontrib>Baharani, Akanksha</creatorcontrib><creatorcontrib>Wei, Zelan</creatorcontrib><creatorcontrib>Truong, Davin</creatorcontrib><creatorcontrib>Bi, Xiaoying</creatorcontrib><creatorcontrib>Wang, Fei</creatorcontrib><creatorcontrib>Li, Xin‐Min</creatorcontrib><creatorcontrib>Verge, Valerie M. K.</creatorcontrib><creatorcontrib>Zhang, Yanbo</creatorcontrib><title>Low field magnetic stimulation promotes myelin repair and cognitive recovery in chronic cuprizone mouse model</title><title>Clinical and experimental pharmacology &amp; physiology</title><addtitle>Clin Exp Pharmacol Physiol</addtitle><description>Background Multiple sclerosis (MS) is an inflammatory demyelinating disease featured with neuroinflammation, demyelination, and the loss of oligodendrocytes. Cognitive impairment and depression are common neuropsychiatric symptoms in MS that are poorly managed with the present interventions. Objective This study aimed to investigate the effects of low field magnetic stimulation (LFMS), a novel non‐invasive neuromodulation technology, on cognitive impairment and depressive symptoms associated with MS using a mouse model of demyelination. Methods C57BL female mice were fed with a 0.2% cuprizone diet for 12 weeks to induce a chronic demyelinating model followed by 4 weeks of cuprizone withdrawal with either sham or LFMS treatment. Results Improved cognition and depression‐like behaviour and restored weight gain were observed in mice with LFMS treatment. Immunohistochemical and immunoblotting data showed enhanced myelin basic protein (MBP) and myelin oligodendrocyte glycoprotein expressions (MOG) in the prefrontal cortex of mice with LFMS treatment, supporting that myelin repair was promoted. LFMS also increased the protein expression of mature oligodendrocyte biomarker glutathione‐S‐transferase (GST‐π). In addition, expression of TGF‐β and associated receptors were elevated with LFMS treatment, implicating this pathway in the response. Conclusion Results from the present study revealed LFMS to have neuroprotective effects, suggesting that LFMS has potential therapeutic value for treating cognitive impairment and depression related to demyelination disorders. Low field magnetic stimulation (LFMS) is a non‐invasive brain stimulation device that improved cognition and depression‐like behaviour and promoted myelin repair and oligodendrocyte maturation in a chronic cuprizone intoxication animal model. The transforming growth factor‐beta signaling pathway may be activated due to LFMS. 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K.</creator><creator>Zhang, Yanbo</creator><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7TK</scope><scope>7U7</scope><scope>C1K</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-2421-157X</orcidid></search><sort><creationdate>202108</creationdate><title>Low field magnetic stimulation promotes myelin repair and cognitive recovery in chronic cuprizone mouse model</title><author>Wang, Zitong ; Baharani, Akanksha ; Wei, Zelan ; Truong, Davin ; Bi, Xiaoying ; Wang, Fei ; Li, Xin‐Min ; Verge, Valerie M. 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K.</creatorcontrib><creatorcontrib>Zhang, Yanbo</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical and experimental pharmacology &amp; physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Zitong</au><au>Baharani, Akanksha</au><au>Wei, Zelan</au><au>Truong, Davin</au><au>Bi, Xiaoying</au><au>Wang, Fei</au><au>Li, Xin‐Min</au><au>Verge, Valerie M. K.</au><au>Zhang, Yanbo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Low field magnetic stimulation promotes myelin repair and cognitive recovery in chronic cuprizone mouse model</atitle><jtitle>Clinical and experimental pharmacology &amp; physiology</jtitle><addtitle>Clin Exp Pharmacol Physiol</addtitle><date>2021-08</date><risdate>2021</risdate><volume>48</volume><issue>8</issue><spage>1090</spage><epage>1102</epage><pages>1090-1102</pages><issn>0305-1870</issn><issn>1440-1681</issn><eissn>1440-1681</eissn><abstract>Background Multiple sclerosis (MS) is an inflammatory demyelinating disease featured with neuroinflammation, demyelination, and the loss of oligodendrocytes. Cognitive impairment and depression are common neuropsychiatric symptoms in MS that are poorly managed with the present interventions. Objective This study aimed to investigate the effects of low field magnetic stimulation (LFMS), a novel non‐invasive neuromodulation technology, on cognitive impairment and depressive symptoms associated with MS using a mouse model of demyelination. Methods C57BL female mice were fed with a 0.2% cuprizone diet for 12 weeks to induce a chronic demyelinating model followed by 4 weeks of cuprizone withdrawal with either sham or LFMS treatment. Results Improved cognition and depression‐like behaviour and restored weight gain were observed in mice with LFMS treatment. Immunohistochemical and immunoblotting data showed enhanced myelin basic protein (MBP) and myelin oligodendrocyte glycoprotein expressions (MOG) in the prefrontal cortex of mice with LFMS treatment, supporting that myelin repair was promoted. LFMS also increased the protein expression of mature oligodendrocyte biomarker glutathione‐S‐transferase (GST‐π). In addition, expression of TGF‐β and associated receptors were elevated with LFMS treatment, implicating this pathway in the response. Conclusion Results from the present study revealed LFMS to have neuroprotective effects, suggesting that LFMS has potential therapeutic value for treating cognitive impairment and depression related to demyelination disorders. Low field magnetic stimulation (LFMS) is a non‐invasive brain stimulation device that improved cognition and depression‐like behaviour and promoted myelin repair and oligodendrocyte maturation in a chronic cuprizone intoxication animal model. The transforming growth factor‐beta signaling pathway may be activated due to LFMS. This study suggests that LFMS has therapeutic potential in demyelinating diseases and related cognitive impairment and depression.</abstract><cop>Australia</cop><pub>Wiley Subscription Services, Inc</pub><pmid>33638234</pmid><doi>10.1111/1440-1681.13490</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-2421-157X</orcidid></addata></record>
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subjects Animals
Biomarkers
Body weight gain
Cognition
Cognitive ability
Cognitive Dysfunction - chemically induced
Cognitive Dysfunction - metabolism
Cognitive Dysfunction - therapy
Cuprizone
Demyelinating diseases
Demyelinating Diseases - chemically induced
Demyelinating Diseases - metabolism
Demyelinating Diseases - therapy
Demyelination
Disease Models, Animal
Female
Glutathione
Glycoproteins
Immunoblotting
Impairment
LFMS
Magnetic Field Therapy - methods
Magnetic fields
Mental depression
Mice
Mice, Inbred C57BL
Multiple sclerosis
Multiple Sclerosis - chemically induced
Multiple Sclerosis - metabolism
Multiple Sclerosis - therapy
Myelin
Myelin basic protein
Myelin Sheath - metabolism
Neuromodulation
Neuroprotection
Oligodendrocyte-myelin glycoprotein
Oligodendrocytes
Prefrontal cortex
Proteins
Recovery of Function
remyelination
Repair
Signs and symptoms
Stimulation
title Low field magnetic stimulation promotes myelin repair and cognitive recovery in chronic cuprizone mouse model
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