REAC technology modifies pathological neuroinflammation and motor behaviour in an Alzheimer’s disease mouse model
The search for new therapeutic approaches to Alzheimer disease (AD) is a major goal in medicine and society, also due to the impressive economic and social costs of this disease. In this scenario, biotechnologies play an important role. Here, it is demonstrated that the Radio Electric Asymmetric Con...
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| Veröffentlicht in: | Scientific reports 2016-10, Vol.6 (1), p.35719-35719, Article 35719 |
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| creator | Lorenzini, Luca Giuliani, Alessandro Sivilia, Sandra Baldassarro, Vito Antonio Fernandez, Mercedes Margotti, Matteo Lotti Giardino, Luciana Fontani, Vania Rinaldi, Salvatore Calzà, Laura |
| description | The search for new therapeutic approaches to Alzheimer disease (AD) is a major goal in medicine and society, also due to the impressive economic and social costs of this disease. In this scenario, biotechnologies play an important role. Here, it is demonstrated that the Radio Electric Asymmetric Conveyer (REAC), an innovative technology platform for neuro- and bio-modulation, used according to the neuro-regenerative protocol (RGN-N), significantly increases astroglial reaction around the amyloid plaques in an AD mouse model, as evaluated by GFAP-immunoreactivity, and reduces microglia-associated neuroinflammation markers, as evaluated by Iba1-immunoreactivity and mRNA expression level of inflammatory cytokines TREM. IL1beta, iNOS and MRC1 were not affected neither by the genotype or by REAC RGN-N treatment. Also observed was an increase in locomotion in treated animals. The study was performed in 24-month-old male Tg2576 mice and age-matching wild-type animals, tested for Y-maze, contextual fear conditioning and locomotion immediately after the end of a specific REAC treatment administered for 15 hours/day for 15 days. These results demonstrated that REAC RGN-N treatment modifies pathological neuroinflammation, and mitigates part of the complex motor behaviour alterations observed in very old Tg2576 mice. |
| doi_str_mv | 10.1038/srep35719 |
| format | Article |
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In this scenario, biotechnologies play an important role. Here, it is demonstrated that the Radio Electric Asymmetric Conveyer (REAC), an innovative technology platform for neuro- and bio-modulation, used according to the neuro-regenerative protocol (RGN-N), significantly increases astroglial reaction around the amyloid plaques in an AD mouse model, as evaluated by GFAP-immunoreactivity, and reduces microglia-associated neuroinflammation markers, as evaluated by Iba1-immunoreactivity and mRNA expression level of inflammatory cytokines TREM. IL1beta, iNOS and MRC1 were not affected neither by the genotype or by REAC RGN-N treatment. Also observed was an increase in locomotion in treated animals. The study was performed in 24-month-old male Tg2576 mice and age-matching wild-type animals, tested for Y-maze, contextual fear conditioning and locomotion immediately after the end of a specific REAC treatment administered for 15 hours/day for 15 days. These results demonstrated that REAC RGN-N treatment modifies pathological neuroinflammation, and mitigates part of the complex motor behaviour alterations observed in very old Tg2576 mice.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/srep35719</identifier><identifier>PMID: 27775040</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/51 ; 38/77 ; 631/378 ; 692/617 ; 82/80 ; Age ; Alzheimer Disease - metabolism ; Alzheimer Disease - pathology ; Alzheimer's disease ; Amyloid ; Amyloid beta-Protein Precursor - metabolism ; Animals ; Biotechnology ; Cytokines - metabolism ; Disease Models, Animal ; Fear conditioning ; Gene expression ; Glial fibrillary acidic protein ; Humanities and Social Sciences ; Immunoreactivity ; Inflammation ; Inflammation - metabolism ; Inflammation - pathology ; Interleukin 1 ; Locomotion ; Male ; Mice ; Mice, Transgenic ; Microglia ; Microglia - metabolism ; Microglia - pathology ; Motor Activity - physiology ; Motor task performance ; multidisciplinary ; Neurodegenerative diseases ; Neuromodulation ; Nitric Oxide Synthase Type II - metabolism ; Nitric-oxide synthase ; Plaque, Amyloid - metabolism ; Plaque, Amyloid - pathology ; RNA, Messenger - metabolism ; Rodents ; Science ; Senile plaques</subject><ispartof>Scientific reports, 2016-10, Vol.6 (1), p.35719-35719, Article 35719</ispartof><rights>The Author(s) 2016</rights><rights>Copyright Nature Publishing Group Oct 2016</rights><rights>Copyright © 2016, The Author(s) 2016 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c438t-2a957dc446916dfce638c824f3e34b5229116bde6df62ef1a2de4685bd175eff3</citedby><cites>FETCH-LOGICAL-c438t-2a957dc446916dfce638c824f3e34b5229116bde6df62ef1a2de4685bd175eff3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5075930/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5075930/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,862,883,27911,27912,41107,42176,51563,53778,53780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27775040$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lorenzini, Luca</creatorcontrib><creatorcontrib>Giuliani, Alessandro</creatorcontrib><creatorcontrib>Sivilia, Sandra</creatorcontrib><creatorcontrib>Baldassarro, Vito Antonio</creatorcontrib><creatorcontrib>Fernandez, Mercedes</creatorcontrib><creatorcontrib>Margotti, Matteo Lotti</creatorcontrib><creatorcontrib>Giardino, Luciana</creatorcontrib><creatorcontrib>Fontani, Vania</creatorcontrib><creatorcontrib>Rinaldi, Salvatore</creatorcontrib><creatorcontrib>Calzà, Laura</creatorcontrib><title>REAC technology modifies pathological neuroinflammation and motor behaviour in an Alzheimer’s disease mouse model</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>The search for new therapeutic approaches to Alzheimer disease (AD) is a major goal in medicine and society, also due to the impressive economic and social costs of this disease. In this scenario, biotechnologies play an important role. Here, it is demonstrated that the Radio Electric Asymmetric Conveyer (REAC), an innovative technology platform for neuro- and bio-modulation, used according to the neuro-regenerative protocol (RGN-N), significantly increases astroglial reaction around the amyloid plaques in an AD mouse model, as evaluated by GFAP-immunoreactivity, and reduces microglia-associated neuroinflammation markers, as evaluated by Iba1-immunoreactivity and mRNA expression level of inflammatory cytokines TREM. IL1beta, iNOS and MRC1 were not affected neither by the genotype or by REAC RGN-N treatment. Also observed was an increase in locomotion in treated animals. The study was performed in 24-month-old male Tg2576 mice and age-matching wild-type animals, tested for Y-maze, contextual fear conditioning and locomotion immediately after the end of a specific REAC treatment administered for 15 hours/day for 15 days. These results demonstrated that REAC RGN-N treatment modifies pathological neuroinflammation, and mitigates part of the complex motor behaviour alterations observed in very old Tg2576 mice.</description><subject>13/51</subject><subject>38/77</subject><subject>631/378</subject><subject>692/617</subject><subject>82/80</subject><subject>Age</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer Disease - pathology</subject><subject>Alzheimer's disease</subject><subject>Amyloid</subject><subject>Amyloid beta-Protein Precursor - metabolism</subject><subject>Animals</subject><subject>Biotechnology</subject><subject>Cytokines - metabolism</subject><subject>Disease Models, Animal</subject><subject>Fear conditioning</subject><subject>Gene expression</subject><subject>Glial fibrillary acidic protein</subject><subject>Humanities and Social Sciences</subject><subject>Immunoreactivity</subject><subject>Inflammation</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lorenzini, Luca</au><au>Giuliani, Alessandro</au><au>Sivilia, Sandra</au><au>Baldassarro, Vito Antonio</au><au>Fernandez, Mercedes</au><au>Margotti, Matteo Lotti</au><au>Giardino, Luciana</au><au>Fontani, Vania</au><au>Rinaldi, Salvatore</au><au>Calzà, Laura</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>REAC technology modifies pathological neuroinflammation and motor behaviour in an Alzheimer’s disease mouse model</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2016-10-24</date><risdate>2016</risdate><volume>6</volume><issue>1</issue><spage>35719</spage><epage>35719</epage><pages>35719-35719</pages><artnum>35719</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>The search for new therapeutic approaches to Alzheimer disease (AD) is a major goal in medicine and society, also due to the impressive economic and social costs of this disease. In this scenario, biotechnologies play an important role. Here, it is demonstrated that the Radio Electric Asymmetric Conveyer (REAC), an innovative technology platform for neuro- and bio-modulation, used according to the neuro-regenerative protocol (RGN-N), significantly increases astroglial reaction around the amyloid plaques in an AD mouse model, as evaluated by GFAP-immunoreactivity, and reduces microglia-associated neuroinflammation markers, as evaluated by Iba1-immunoreactivity and mRNA expression level of inflammatory cytokines TREM. IL1beta, iNOS and MRC1 were not affected neither by the genotype or by REAC RGN-N treatment. Also observed was an increase in locomotion in treated animals. The study was performed in 24-month-old male Tg2576 mice and age-matching wild-type animals, tested for Y-maze, contextual fear conditioning and locomotion immediately after the end of a specific REAC treatment administered for 15 hours/day for 15 days. These results demonstrated that REAC RGN-N treatment modifies pathological neuroinflammation, and mitigates part of the complex motor behaviour alterations observed in very old Tg2576 mice.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>27775040</pmid><doi>10.1038/srep35719</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13/51 38/77 631/378 692/617 82/80 Age Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer's disease Amyloid Amyloid beta-Protein Precursor - metabolism Animals Biotechnology Cytokines - metabolism Disease Models, Animal Fear conditioning Gene expression Glial fibrillary acidic protein Humanities and Social Sciences Immunoreactivity Inflammation Inflammation - metabolism Inflammation - pathology Interleukin 1 Locomotion Male Mice Mice, Transgenic Microglia Microglia - metabolism Microglia - pathology Motor Activity - physiology Motor task performance multidisciplinary Neurodegenerative diseases Neuromodulation Nitric Oxide Synthase Type II - metabolism Nitric-oxide synthase Plaque, Amyloid - metabolism Plaque, Amyloid - pathology RNA, Messenger - metabolism Rodents Science Senile plaques |
| title | REAC technology modifies pathological neuroinflammation and motor behaviour in an Alzheimer’s disease mouse model |
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