Long-term exposure to ELF-MF ameliorates cognitive deficits and attenuates tau hyperphosphorylation in 3xTg AD mice
•ELF-MF exposure ameliorate cognitive deficits in AD mice.•Tau hyperphosphorylation was also attenuated in AD mice.•ELF-MF treatment maybe a new means to cure AD Although numerous studies have reported the influence of extremely low frequency magnetic field (ELF-MF) exposure on human health, its eff...
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| Veröffentlicht in: | Neurotoxicology (Park Forest South) 2016-03, Vol.53, p.290-300 |
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| creator | Hu, Yu Lai, Jinsheng Wan, Baoquan Liu, Xingfa Zhang, Yemao Zhang, Jiangong Sun, Dongsheng Ruan, Guoran Liu, Enjie Liu, Gong-Ping Chen, Chen Wang, Dao Wen |
| description | •ELF-MF exposure ameliorate cognitive deficits in AD mice.•Tau hyperphosphorylation was also attenuated in AD mice.•ELF-MF treatment maybe a new means to cure AD
Although numerous studies have reported the influence of extremely low frequency magnetic field (ELF-MF) exposure on human health, its effects on cognitive deficits in Alzheimer’s disease (AD) have remained under debate. Moreover, the influence of ELF-MF on hyperphosphorylated tau, which is one of the most common pathological hallmarks of AD, has not been reported to date. Therefore, transgenic mice (3xTg) were used in the present study. 3xTg mice, which express an APP/PS1 mutation combined with a tau (P301L) mutation and that develop cognitive deficits at 6 months of age, were subjected to ELF-MF (50Hz, 500μT) exposure or sham exposure daily for 3 months. We discovered that ELF-MF exposure ameliorated cognitive deficits and increased synaptic proteins in 3xTg mice. The protective effects of ELF-MF exposure may have also been caused by the inhibition of apoptosis and/or decreased oxidative stress levels that were observed in the hippocampus tissues of treated mice. Furthermore, tau hyperphosphorylation was decreased in vivo because of ELF-MF exposure, and this decrease was induced by the inhibition of GSK3β and CDK5 activities and activation of PP2Ac. We are the first to report that exposure to ELF-MF can attenuate tau phosphorylation. These findings suggest that ELF-MF exposure could act as a valid therapeutic strategy for ameliorating cognitive deficits and attenuating tau hyperphosphorylation in AD. |
| doi_str_mv | 10.1016/j.neuro.2016.02.012 |
| format | Article |
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Although numerous studies have reported the influence of extremely low frequency magnetic field (ELF-MF) exposure on human health, its effects on cognitive deficits in Alzheimer’s disease (AD) have remained under debate. Moreover, the influence of ELF-MF on hyperphosphorylated tau, which is one of the most common pathological hallmarks of AD, has not been reported to date. Therefore, transgenic mice (3xTg) were used in the present study. 3xTg mice, which express an APP/PS1 mutation combined with a tau (P301L) mutation and that develop cognitive deficits at 6 months of age, were subjected to ELF-MF (50Hz, 500μT) exposure or sham exposure daily for 3 months. We discovered that ELF-MF exposure ameliorated cognitive deficits and increased synaptic proteins in 3xTg mice. The protective effects of ELF-MF exposure may have also been caused by the inhibition of apoptosis and/or decreased oxidative stress levels that were observed in the hippocampus tissues of treated mice. Furthermore, tau hyperphosphorylation was decreased in vivo because of ELF-MF exposure, and this decrease was induced by the inhibition of GSK3β and CDK5 activities and activation of PP2Ac. We are the first to report that exposure to ELF-MF can attenuate tau phosphorylation. These findings suggest that ELF-MF exposure could act as a valid therapeutic strategy for ameliorating cognitive deficits and attenuating tau hyperphosphorylation in AD.</description><identifier>ISSN: 0161-813X</identifier><identifier>EISSN: 1872-9711</identifier><identifier>DOI: 10.1016/j.neuro.2016.02.012</identifier><identifier>PMID: 26945731</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Alzheimer Disease - complications ; Alzheimer Disease - genetics ; Alzheimer Disease - radiotherapy ; Alzheimer’s disease ; Amyloid beta-Protein Precursor - genetics ; Animals ; Apoptosis - genetics ; Apoptosis - radiation effects ; Cognition Disorders - etiology ; Cognition Disorders - therapy ; Cognitive ; Conditioning (Psychology) - physiology ; Conditioning (Psychology) - radiation effects ; Cyclin-Dependent Kinase 5 - genetics ; Cyclin-Dependent Kinase 5 - metabolism ; Disease Models, Animal ; Dose-Response Relationship, Radiation ; ELF-MF ; Gene Expression Regulation - genetics ; Gene Expression Regulation - radiation effects ; Glycogen Synthase Kinase 3 beta - genetics ; Glycogen Synthase Kinase 3 beta - metabolism ; Humans ; Magnetic Field Therapy - methods ; Maze Learning - physiology ; Maze Learning - radiation effects ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutation - genetics ; Phosphorylation - radiation effects ; Presenilin-1 - genetics ; Reactive Oxygen Species - metabolism ; Tau phosphorylation ; tau Proteins - genetics ; tau Proteins - metabolism</subject><ispartof>Neurotoxicology (Park Forest South), 2016-03, Vol.53, p.290-300</ispartof><rights>2016 Elsevier Inc.</rights><rights>Copyright © 2016 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c392t-58b22d7afac27187c495b64424540748559eba6e431f12e8e9bff8d9ec8f3ba03</citedby><cites>FETCH-LOGICAL-c392t-58b22d7afac27187c495b64424540748559eba6e431f12e8e9bff8d9ec8f3ba03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0161813X16300237$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26945731$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hu, Yu</creatorcontrib><creatorcontrib>Lai, Jinsheng</creatorcontrib><creatorcontrib>Wan, Baoquan</creatorcontrib><creatorcontrib>Liu, Xingfa</creatorcontrib><creatorcontrib>Zhang, Yemao</creatorcontrib><creatorcontrib>Zhang, Jiangong</creatorcontrib><creatorcontrib>Sun, Dongsheng</creatorcontrib><creatorcontrib>Ruan, Guoran</creatorcontrib><creatorcontrib>Liu, Enjie</creatorcontrib><creatorcontrib>Liu, Gong-Ping</creatorcontrib><creatorcontrib>Chen, Chen</creatorcontrib><creatorcontrib>Wang, Dao Wen</creatorcontrib><title>Long-term exposure to ELF-MF ameliorates cognitive deficits and attenuates tau hyperphosphorylation in 3xTg AD mice</title><title>Neurotoxicology (Park Forest South)</title><addtitle>Neurotoxicology</addtitle><description>•ELF-MF exposure ameliorate cognitive deficits in AD mice.•Tau hyperphosphorylation was also attenuated in AD mice.•ELF-MF treatment maybe a new means to cure AD
Although numerous studies have reported the influence of extremely low frequency magnetic field (ELF-MF) exposure on human health, its effects on cognitive deficits in Alzheimer’s disease (AD) have remained under debate. Moreover, the influence of ELF-MF on hyperphosphorylated tau, which is one of the most common pathological hallmarks of AD, has not been reported to date. Therefore, transgenic mice (3xTg) were used in the present study. 3xTg mice, which express an APP/PS1 mutation combined with a tau (P301L) mutation and that develop cognitive deficits at 6 months of age, were subjected to ELF-MF (50Hz, 500μT) exposure or sham exposure daily for 3 months. We discovered that ELF-MF exposure ameliorated cognitive deficits and increased synaptic proteins in 3xTg mice. The protective effects of ELF-MF exposure may have also been caused by the inhibition of apoptosis and/or decreased oxidative stress levels that were observed in the hippocampus tissues of treated mice. Furthermore, tau hyperphosphorylation was decreased in vivo because of ELF-MF exposure, and this decrease was induced by the inhibition of GSK3β and CDK5 activities and activation of PP2Ac. We are the first to report that exposure to ELF-MF can attenuate tau phosphorylation. These findings suggest that ELF-MF exposure could act as a valid therapeutic strategy for ameliorating cognitive deficits and attenuating tau hyperphosphorylation in AD.</description><subject>Alzheimer Disease - complications</subject><subject>Alzheimer Disease - genetics</subject><subject>Alzheimer Disease - radiotherapy</subject><subject>Alzheimer’s disease</subject><subject>Amyloid beta-Protein Precursor - genetics</subject><subject>Animals</subject><subject>Apoptosis - genetics</subject><subject>Apoptosis - radiation effects</subject><subject>Cognition Disorders - etiology</subject><subject>Cognition Disorders - therapy</subject><subject>Cognitive</subject><subject>Conditioning (Psychology) - physiology</subject><subject>Conditioning (Psychology) - radiation effects</subject><subject>Cyclin-Dependent Kinase 5 - genetics</subject><subject>Cyclin-Dependent Kinase 5 - metabolism</subject><subject>Disease Models, Animal</subject><subject>Dose-Response Relationship, Radiation</subject><subject>ELF-MF</subject><subject>Gene Expression Regulation - genetics</subject><subject>Gene Expression Regulation - radiation effects</subject><subject>Glycogen Synthase Kinase 3 beta - genetics</subject><subject>Glycogen Synthase Kinase 3 beta - metabolism</subject><subject>Humans</subject><subject>Magnetic Field Therapy - methods</subject><subject>Maze Learning - physiology</subject><subject>Maze Learning - radiation effects</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Mutation - genetics</subject><subject>Phosphorylation - radiation effects</subject><subject>Presenilin-1 - genetics</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Tau phosphorylation</subject><subject>tau Proteins - genetics</subject><subject>tau Proteins - metabolism</subject><issn>0161-813X</issn><issn>1872-9711</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU1v1DAQhi0EokvhFyAhH7kk9Vfi-MChKl1AWsSlSNwsx5lsvUrsYDtV99_jdgvHioNlWfPMvBo_CL2npKaEtheH2sMaQ83KoyasJpS9QBvaSVYpSelLtCkFWnWU_zpDb1I6EEIb2arX6Iy1SjSS0w1Ku-D3VYY4Y7hfQloj4Bzw9W5bfd9iM8PkQjQZErZh7112d4AHGJ11OWHjB2xyBr8-Etms-Pa4QFxuQyonHieTXfDYeczvb_b48jOenYW36NVopgTvnu5z9HN7fXP1tdr9-PLt6nJXWa5YrpquZ2yQZjSWybKWFarpWyGYaASRomsaBb1pQXA6UgYdqH4cu0GB7UbeG8LP0cfT3CWG3yukrGeXLEyT8RDWpKnsGiZEmf0fqGyJ4lLQgvITamNIKcKol-hmE4-aEv0gRh_0oxj9IEYTpouY0vXhKWDtZxj-9fw1UYBPJwDKj9w5iDpZB97C4CLYrIfgng34A6xmoNo</recordid><startdate>201603</startdate><enddate>201603</enddate><creator>Hu, Yu</creator><creator>Lai, Jinsheng</creator><creator>Wan, Baoquan</creator><creator>Liu, Xingfa</creator><creator>Zhang, Yemao</creator><creator>Zhang, Jiangong</creator><creator>Sun, Dongsheng</creator><creator>Ruan, Guoran</creator><creator>Liu, Enjie</creator><creator>Liu, Gong-Ping</creator><creator>Chen, Chen</creator><creator>Wang, Dao Wen</creator><general>Elsevier B.V</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>7X8</scope><scope>7TK</scope><scope>7U7</scope><scope>C1K</scope></search><sort><creationdate>201603</creationdate><title>Long-term exposure to ELF-MF ameliorates cognitive deficits and attenuates tau hyperphosphorylation in 3xTg AD mice</title><author>Hu, Yu ; Lai, Jinsheng ; Wan, Baoquan ; Liu, Xingfa ; Zhang, Yemao ; Zhang, Jiangong ; Sun, Dongsheng ; Ruan, Guoran ; Liu, Enjie ; Liu, Gong-Ping ; Chen, Chen ; Wang, Dao Wen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c392t-58b22d7afac27187c495b64424540748559eba6e431f12e8e9bff8d9ec8f3ba03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Alzheimer Disease - complications</topic><topic>Alzheimer Disease - genetics</topic><topic>Alzheimer Disease - radiotherapy</topic><topic>Alzheimer’s disease</topic><topic>Amyloid beta-Protein Precursor - genetics</topic><topic>Animals</topic><topic>Apoptosis - genetics</topic><topic>Apoptosis - radiation effects</topic><topic>Cognition Disorders - etiology</topic><topic>Cognition Disorders - therapy</topic><topic>Cognitive</topic><topic>Conditioning (Psychology) - physiology</topic><topic>Conditioning (Psychology) - radiation effects</topic><topic>Cyclin-Dependent Kinase 5 - genetics</topic><topic>Cyclin-Dependent Kinase 5 - metabolism</topic><topic>Disease Models, Animal</topic><topic>Dose-Response Relationship, Radiation</topic><topic>ELF-MF</topic><topic>Gene Expression Regulation - genetics</topic><topic>Gene Expression Regulation - radiation effects</topic><topic>Glycogen Synthase Kinase 3 beta - genetics</topic><topic>Glycogen Synthase Kinase 3 beta - metabolism</topic><topic>Humans</topic><topic>Magnetic Field Therapy - methods</topic><topic>Maze Learning - physiology</topic><topic>Maze Learning - radiation effects</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Mutation - genetics</topic><topic>Phosphorylation - radiation effects</topic><topic>Presenilin-1 - genetics</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Tau phosphorylation</topic><topic>tau Proteins - genetics</topic><topic>tau Proteins - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hu, Yu</creatorcontrib><creatorcontrib>Lai, Jinsheng</creatorcontrib><creatorcontrib>Wan, Baoquan</creatorcontrib><creatorcontrib>Liu, Xingfa</creatorcontrib><creatorcontrib>Zhang, Yemao</creatorcontrib><creatorcontrib>Zhang, Jiangong</creatorcontrib><creatorcontrib>Sun, Dongsheng</creatorcontrib><creatorcontrib>Ruan, Guoran</creatorcontrib><creatorcontrib>Liu, Enjie</creatorcontrib><creatorcontrib>Liu, Gong-Ping</creatorcontrib><creatorcontrib>Chen, Chen</creatorcontrib><creatorcontrib>Wang, Dao Wen</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Neurotoxicology (Park Forest South)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hu, Yu</au><au>Lai, Jinsheng</au><au>Wan, Baoquan</au><au>Liu, Xingfa</au><au>Zhang, Yemao</au><au>Zhang, Jiangong</au><au>Sun, Dongsheng</au><au>Ruan, Guoran</au><au>Liu, Enjie</au><au>Liu, Gong-Ping</au><au>Chen, Chen</au><au>Wang, Dao Wen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Long-term exposure to ELF-MF ameliorates cognitive deficits and attenuates tau hyperphosphorylation in 3xTg AD mice</atitle><jtitle>Neurotoxicology (Park Forest South)</jtitle><addtitle>Neurotoxicology</addtitle><date>2016-03</date><risdate>2016</risdate><volume>53</volume><spage>290</spage><epage>300</epage><pages>290-300</pages><issn>0161-813X</issn><eissn>1872-9711</eissn><abstract>•ELF-MF exposure ameliorate cognitive deficits in AD mice.•Tau hyperphosphorylation was also attenuated in AD mice.•ELF-MF treatment maybe a new means to cure AD
Although numerous studies have reported the influence of extremely low frequency magnetic field (ELF-MF) exposure on human health, its effects on cognitive deficits in Alzheimer’s disease (AD) have remained under debate. Moreover, the influence of ELF-MF on hyperphosphorylated tau, which is one of the most common pathological hallmarks of AD, has not been reported to date. Therefore, transgenic mice (3xTg) were used in the present study. 3xTg mice, which express an APP/PS1 mutation combined with a tau (P301L) mutation and that develop cognitive deficits at 6 months of age, were subjected to ELF-MF (50Hz, 500μT) exposure or sham exposure daily for 3 months. We discovered that ELF-MF exposure ameliorated cognitive deficits and increased synaptic proteins in 3xTg mice. The protective effects of ELF-MF exposure may have also been caused by the inhibition of apoptosis and/or decreased oxidative stress levels that were observed in the hippocampus tissues of treated mice. Furthermore, tau hyperphosphorylation was decreased in vivo because of ELF-MF exposure, and this decrease was induced by the inhibition of GSK3β and CDK5 activities and activation of PP2Ac. We are the first to report that exposure to ELF-MF can attenuate tau phosphorylation. These findings suggest that ELF-MF exposure could act as a valid therapeutic strategy for ameliorating cognitive deficits and attenuating tau hyperphosphorylation in AD.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>26945731</pmid><doi>10.1016/j.neuro.2016.02.012</doi><tpages>11</tpages></addata></record> |
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| ispartof | Neurotoxicology (Park Forest South), 2016-03, Vol.53, p.290-300 |
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| subjects | Alzheimer Disease - complications Alzheimer Disease - genetics Alzheimer Disease - radiotherapy Alzheimer’s disease Amyloid beta-Protein Precursor - genetics Animals Apoptosis - genetics Apoptosis - radiation effects Cognition Disorders - etiology Cognition Disorders - therapy Cognitive Conditioning (Psychology) - physiology Conditioning (Psychology) - radiation effects Cyclin-Dependent Kinase 5 - genetics Cyclin-Dependent Kinase 5 - metabolism Disease Models, Animal Dose-Response Relationship, Radiation ELF-MF Gene Expression Regulation - genetics Gene Expression Regulation - radiation effects Glycogen Synthase Kinase 3 beta - genetics Glycogen Synthase Kinase 3 beta - metabolism Humans Magnetic Field Therapy - methods Maze Learning - physiology Maze Learning - radiation effects Mice Mice, Inbred C57BL Mice, Transgenic Mutation - genetics Phosphorylation - radiation effects Presenilin-1 - genetics Reactive Oxygen Species - metabolism Tau phosphorylation tau Proteins - genetics tau Proteins - metabolism |
| title | Long-term exposure to ELF-MF ameliorates cognitive deficits and attenuates tau hyperphosphorylation in 3xTg AD mice |
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