{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,3]],"date-time":"2026-08-03T17:43:27Z","timestamp":1785779007974,"version":"3.56.0"},"reference-count":50,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2023,1,11]],"date-time":"2023-01-11T00:00:00Z","timestamp":1673395200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100004543","name":"China Scholarship Council","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100004543","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2023,2]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Alzheimer's disease (AD) and Parkinson's disease (PD) are age\u2010dependent neurodegenerative disorders. There is a profound neuronal loss in the basal forebrain cholinergic system in AD and severe dopaminergic deficiency within the nigrostriatal pathway in PD. Swedish APP (APP\n                    <jats:sub>SWE<\/jats:sub>\n                    ) and SNCA\n                    <jats:sub>A53T<\/jats:sub>\n                    mutations promote A\u03b2 generation and \u03b1\u2010synuclein aggregation, respectively, and have been linked to the pathogenesis of AD and PD. However, the mechanisms underlying selective cholinergic and dopaminergic neurodegeneration in AD and PD are still unknown. We demonstrated that APP\n                    <jats:sub>SWE<\/jats:sub>\n                    mutation enhanced A\u03b2 generation and increased cell susceptibility to A\u03b2 oligomer in cholinergic SN56 cells, whereas SNCA\n                    <jats:sub>A53T<\/jats:sub>\n                    mutations promoted aggregates formation and potentiated mutant \u03b1\u2010synuclein oligomer\u2010induced cytotoxicity in MN9D cells. Furthermore, syndecan\u20103 (SDC3) and fibroblast growth factor receptor\u2010like 1 (FGFRL1) genes were differentially expressed in SN56 and MN9D cells carrying APP\n                    <jats:sub>SWE<\/jats:sub>\n                    or SNCA\n                    <jats:sub>A53T<\/jats:sub>\n                    mutation. SDC3 and FGFRL1 proteins were preferentially expressed in the cholinergic nucleus and dopaminergic neurons of APP\n                    <jats:sub>SWE<\/jats:sub>\n                    and SNCA\n                    <jats:sub>A53T<\/jats:sub>\n                    mouse models, respectively. Finally, the knockdown of SDC3 and FGFRL1 attenuated oxidative stress\u2010induced cell death in SN56\u2010APP\n                    <jats:sub>SWE<\/jats:sub>\n                    and MN9D\u2010SNCAA53T cells. The results demonstrate that SDC3 and FGFRL1 mediated the specific effects of APP\n                    <jats:sub>SWE<\/jats:sub>\n                    and SNCA\n                    <jats:sub>A53T<\/jats:sub>\n                    on cholinergic and dopaminergic neurodegeneration in AD and PD, respectively. Our study suggests that SDC3 and FGFRL1 could be potential targets to alleviate the selective neurodegeneration in AD and PD.\n                  <\/jats:p>","DOI":"10.1096\/fj.202201359r","type":"journal-article","created":{"date-parts":[[2023,1,11]],"date-time":"2023-01-11T10:26:34Z","timestamp":1673432794000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Distinct effects of\n                    <scp>SDC3<\/scp>\n                    and\n                    <scp>FGFRL1<\/scp>\n                    on selective neurodegeneration in\n                    <scp>AD<\/scp>\n                    and\n                    <scp>PD<\/scp>"],"prefix":"10.1096","volume":"37","author":[{"given":"Juelu","family":"Wang","sequence":"first","affiliation":[{"name":"Townsend Family Laboratories, Department of Psychiatry, Graduate Program in Neuroscience The University of British Columbia  Vancouver British Columbia 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