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Delivery of neurotrophins may potentially revive degenerating motor neurons, yet this approach is dependent on the proper subcellular localization of neurotrophin receptor (NTR) to plasmalemmal signaling microdomains, termed membrane\/lipid rafts (MLRs). We previously showed that over\u2010expression of synapsin\u2010driven caveolin\u20101 (Cav\u20101) (\n                    <jats:italic>SynCav1<\/jats:italic>\n                    ) increases MLR localization of NTR\n                    <jats:italic>[e.g<\/jats:italic>\n                    ., receptor tyrosine kinase B (TrkB)], promotes hippocampal synaptic and neuroplasticity, and significantly improves learning and memory in aged mice. The present study crossed a SynCav1 transgene\u2010positive (SynCav1\n                    <jats:sup>+<\/jats:sup>\n                    ) mouse with the mutant human superoxide dismutase glycine to alanine point mutation at amino acid 93 (hSOD1\n                    <jats:sup>G93A<\/jats:sup>\n                    ) mouse model of ALS. When compared with hSOD1\n                    <jats:sup>G93A<\/jats:sup>\n                    , hSOD1\n                    <jats:sup>G93A<\/jats:sup>\n                    \/SynCav1\n                    <jats:sup>+<\/jats:sup>\n                    mice exhibited greater body weight and longer survival as well as better motor function. Microscopic analyses of hSOD1\n                    <jats:sup>G93A<\/jats:sup>\n                    \/SynCav1\n                    <jats:sup>+<\/jats:sup>\n                    spinal cords revealed preserved spinal cord \u03b1\u2010motor neurons and preserved mitochondrial morphology. Moreover, hSOD1\n                    <jats:sup>G93A<\/jats:sup>\n                    \/SynCav1\n                    <jats:sup>+<\/jats:sup>\n                    spinal cords contained more MLRs (cholera toxin subunit B positive) and MLR\u2010associated TrkB and Cav\u20101 protein expression. These findings demonstrate that\n                    <jats:italic>SynCav1<\/jats:italic>\n                    delays disease progression in a mouse model of ALS, potentially by preserving or restoring NTR expression and localization to MLRs.\u2014Sawada, A., Wang, S., Jian, M., Leem, J., Wackerbarth, J., Egawa, J., Schilling, J. M., Platoshyn, O., Zemljic\u2010Harpf, A., Roth, D. M., Patel, H. H., Patel, P. M., Marsala, M., Head, B. P. Neuron\u2010targeted caveolin\u20101 improves neuromuscular function and extends survival in SOD1\n                    <jats:sup>G93A<\/jats:sup>\n                    mice. FASEB J. 33, 7545\u20137554 (2019).\n                    <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/www.fasebj.org\">www.fasebj.org<\/jats:ext-link>\n                  <\/jats:p>","DOI":"10.1096\/fj.201802652rr","type":"journal-article","created":{"date-parts":[[2019,3,20]],"date-time":"2019-03-20T21:27:07Z","timestamp":1553117227000},"page":"7545-7554","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":35,"title":["Neuron\u2010targeted caveolin\u20101 improves neuromuscular function and extends survival in SOD1\n                    <sup>G93A<\/sup>\n                    mice"],"prefix":"10.1096","volume":"33","author":[{"given":"Atsushi","family":"Sawada","sequence":"first","affiliation":[{"name":"Veterans Affairs San Diego Healthcare System San Diego California USA"},{"name":"Department of Anesthesiology School of Medicine University of California-San Diego La Jolla California 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