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Lesion development in MS is associated with increased expression of FGF1, FGF2 and FGF9, all of which modulate remyelination in a variety of experimental settings. However, FGF9 is also selectively upregulated in major depressive disorder (MDD), prompting us to speculate it may also have a direct effect on neuronal function and survival.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Transcriptional profiling of myelinating cultures treated with FGF1, FGF2 or FGF9 was performed, and the effects of FGF9 on cortical neurons investigated using a combination of transcriptional, electrophysiological and immunofluorescence microscopic techniques. The in vivo effects of FGF9 were explored by stereotactic injection of adeno\u2010associated viral (AAV) vectors encoding either FGF9 or EGFP into the rat motor cortex.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Transcriptional profiling of myelinating cultures after FGF9 treatment revealed a distinct neuronal response with a pronounced downregulation of gene networks associated with axonal transport and synaptic function. In cortical neuronal cultures, FGF9 also rapidly downregulated expression of genes associated with synaptic function. This was associated with a complete block in the development of photo\u2010inducible spiking activity, as demonstrated using multi\u2010electrode recordings of channel rhodopsin\u2010transfected rat cortical neurons in vitro and, ultimately, neuronal cell death. Overexpression of FGF9 in vivo resulted in rapid loss of neurons and subsequent development of chronic grey matter lesions with neuroaxonal reduction and ensuing myelin loss.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>These observations identify overexpression of FGF9 as a mechanism by which neuroaxonal pathology could develop independently of immune\u2010mediated demyelination in MS. We suggest targeting neuronal FGF9\u2010dependent pathways may provide a novel strategy to slow if not halt neuroaxonal atrophy and loss in MS, MDD and potentially other neurodegenerative diseases.<\/jats:p><\/jats:sec>","DOI":"10.1111\/nan.12935","type":"journal-article","created":{"date-parts":[[2023,9,14]],"date-time":"2023-09-14T04:34:00Z","timestamp":1694666040000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Fibroblast growth factor 9 (FGF9)\u2010mediated neurodegeneration: Implications for progressive multiple sclerosis?"],"prefix":"10.1111","volume":"49","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1681-2359","authenticated-orcid":false,"given":"Katja","family":"Th\u00fcmmler","sequence":"first","affiliation":[{"name":"School of Infection and Immunity University of Glasgow  Glasgow 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