{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T11:47:16Z","timestamp":1791805636903,"version":"4.3.4"},"reference-count":50,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T00:00:00Z","timestamp":1791763200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T00:00:00Z","timestamp":1791763200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Annals of Neurology"],"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Early phenotypic presentation of central afferent synapse dysfunction within patients with spinal muscular atrophy (SMA) represents a key target for therapeutic development; however, the underlying disease mechanisms remain unresolved. By further investigating motor neuron synapse and peri\u2010synaptic astrocyte process (PAP) defects in human SMA disease pathology, we aimed to develop a novel therapeutic approach to improve motor neuron function.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We utilized healthy subjects and patients with SMA induced pluripotent stem cell (iPSC)\u2010derived cultures to assess phenotypes occurring intrinsically within astrocyte processes (monocultures) and at the PAP\u2010synaptic interface (co\u2010cultures), respectively, using cell surface capture mass spectrometry proteomics, confocal and super resolution microscopy, synaptogliosome (SG) isolation, and electrophysiology.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>SMA astrocytes demonstrated intrinsic filopodia actin defects featuring low abundance of actin\u2010associated cell surface N\u2010glycoproteins, decreased filopodia density and CDC42\u2010GTP levels after actin remodeling stimulation, and significantly reduced phosphorylated ezrin, radixin, and moesin (pERM) proteins. Within the SMA motor neuron and astrocyte co\u2010cultures, we observed concurrent decreases in synapse number, actin\u2010associated synapsin I expression, and PAP\u2010associated expression of pERM proteins. Our dual treatment paradigm using SMN1 gene therapy combined with forskolin treatment to stimulate actin dynamics via increasing cyclic adenosine monophosphate levels resulted in increased branching and filopodia density of SMA astrocytes, and improved synapse formation and function of SMA motor neurons.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Interpretation<\/jats:title>\n                    <jats:p>We define actin\u2010associated defects impacting astrocyte filopodia dynamics and motor neuron synaptic function in SMA. This shaped our therapeutic approach targeted to SMN\u2010dependent and actin\u2010related disease mechanisms, which overall demonstrated improvements in motor neuron function and disease pathology. ANN NEUROL 2026<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ana.78390","type":"journal-article","created":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T11:06:43Z","timestamp":1791803203000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Astrocyte\n                    <scp>SMN<\/scp>\n                    Restoration and Forskolin Treatment Improve\n                    <scp>SMA<\/scp>\n                    Synaptic Pathology"],"prefix":"10.1002","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2408-0407","authenticated-orcid":false,"given":"Emily","family":"Welby","sequence":"first","affiliation":[{"name":"Department of Cell Biology, Neurobiology, and Anatomy, Neuroscience Research Center Medical College of Wisconsin  Milwaukee WI USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaojie","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology Medical College of Wisconsin  Milwaukee WI USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melinda","family":"Wojtkiewicz","sequence":"additional","affiliation":[{"name":"Department of Cellular and Integrative Physiology, and CardiOmics Program, Center for Heart and Vascular Research University of Nebraska Medical Center  Omaha NE USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Linda Berg","family":"Luecke","sequence":"additional","affiliation":[{"name":"Department of Cellular and Integrative Physiology, and CardiOmics Program, Center for Heart and Vascular Research University of Nebraska Medical Center  Omaha NE USA"},{"name":"Department of Biochemistry Medical College of Wisconsin  Milwaukee WI USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rebekah L.","family":"Gundry","sequence":"additional","affiliation":[{"name":"Department of Cellular and Integrative Physiology, and CardiOmics Program, Center for Heart and Vascular Research University of Nebraska Medical Center  Omaha NE USA"},{"name":"Department of Biochemistry Medical College of Wisconsin  Milwaukee WI USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qing\u2010Song","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology Medical College of Wisconsin  Milwaukee WI USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9676-8548","authenticated-orcid":false,"given":"Allison D.","family":"Ebert","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, Neurobiology, and Anatomy, Neuroscience Research Center Medical College of Wisconsin  Milwaukee WI 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