{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,12]],"date-time":"2026-09-12T03:12:02Z","timestamp":1789182722100,"version":"build-2803163510"},"reference-count":48,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2016,4,12]],"date-time":"2016-04-12T00:00:00Z","timestamp":1460419200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100000646","name":"Japan Society for the Promotion of Science London","doi-asserted-by":"publisher","award":["25\u20105321"],"award-info":[{"award-number":["25\u20105321"]}],"id":[{"id":"10.13039\/501100000646","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurochemistry"],"published-print":{"date-parts":[[2016,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:label\/><jats:p>Parkinson's disease (<jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>) is a progressive neurodegenerative disorder that is characterized by the selective loss of dopaminergic neurons in the substantia nigra pars compacta (<jats:styled-content style=\"fixed-case\">SN<\/jats:styled-content>c). Several lines of evidence suggest that neurodegeneration in <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content> is accelerated by a vicious cycle in which apoptosis in dopaminergic neurons triggers the activation of microglia and harmful inflammatory processes that further amplify neuronal death. Recently, we demonstrated that the deletion of collapsin response mediator protein 4 (<jats:styled-content style=\"fixed-case\">CRMP<\/jats:styled-content>4) suppresses inflammatory responses and cell death in a mouse model of spinal cord injury, leading to improved functional recovery. We thus hypothesized that <jats:italic>Crmp4<\/jats:italic>\u2212\/\u2212 mice may have limited inflammatory responses and a decrease in the loss of <jats:styled-content style=\"fixed-case\">SN<\/jats:styled-content>c dopaminergic neurons in an 1\u2010methyl\u20104\u2010phenyl\u20101,2,3,6\u2010tetrahydropyridine (<jats:styled-content style=\"fixed-case\">MPTP<\/jats:styled-content>)\u2010induced <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content> mouse model. We observed <jats:styled-content style=\"fixed-case\">CRMP<\/jats:styled-content>4 expression in neurons, astrocytes, and microglia\/macrophages following the injection of 25\u00a0mg\/kg <jats:styled-content style=\"fixed-case\">MPTP<\/jats:styled-content>. We compared the number of dopaminergic neurons and the inflammatory response in <jats:styled-content style=\"fixed-case\">SN<\/jats:styled-content>c between <jats:italic>Crmp4<\/jats:italic>+\/+ and <jats:italic>Crmp4<\/jats:italic>\u2212\/\u2212 mice after <jats:styled-content style=\"fixed-case\">MPTP<\/jats:styled-content> injection. Limited loss of <jats:styled-content style=\"fixed-case\">SN<\/jats:styled-content>c dopaminergic neurons and decreased activations of microglia and astrocytes were observed in <jats:italic>Crmp4<\/jats:italic>\u2212\/\u2212 mice. These results suggest that <jats:styled-content style=\"fixed-case\">CRMP<\/jats:styled-content>4 is a novel therapeutic target in the treatment of <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content> patients.<\/jats:p><\/jats:sec><jats:sec><jats:label\/><jats:p>\n<jats:boxed-text content-type=\"graphic\" position=\"anchor\"><jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/jnc13617-fig-0007-m.png\"><jats:alt-text>image<\/jats:alt-text><\/jats:graphic><\/jats:boxed-text>We demonstrated that genetic CRMP4 deletion delays a vicious cycle of inflammation and neurodegeneration in a Parkinson's disease mouse model. MPTP (1\u2010methyl\u20104\u2010phenyl\u20101,2,3,6\u2010tetrahydropyridine) injection to wild\u2010type mice induces collapsin response mediator protein 4 (CRMP4) up\u2010regulation in neurons, astrocytes, and microglia. CRMP4\u2010deficient mice show reduced inflammation and suppressed dopaminergic neuronal death after MPTP injection. These findings suggest that CRMP4 deletion may be a new therapeutic strategy against Parkinson's diseases.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jnc.13617","type":"journal-article","created":{"date-parts":[[2016,3,19]],"date-time":"2016-03-19T02:04:51Z","timestamp":1458353091000},"page":"795-805","source":"Crossref","is-referenced-by-count":13,"title":["Loss of collapsin response mediator protein 4 suppresses dopaminergic neuron death in an 1\u2010methyl\u20104\u2010phenyl\u20101,2,3,6\u2010tetrahydropyridine\u2010induced mouse model of Parkinson's disease"],"prefix":"10.1111","volume":"137","author":[{"given":"Aine","family":"Tonouchi","sequence":"first","affiliation":[{"name":"Department of Life Science and Medical Bioscience Graduate School of Advanced Science and Engineering Waseda University Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun","family":"Nagai","sequence":"additional","affiliation":[{"name":"Department of Life Science and Medical 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