{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,2,9]],"date-time":"2026-02-09T17:08:52Z","timestamp":1770656932935,"version":"3.49.0"},"posted":{"date-parts":[[2026,1,27]]},"group-title":"Neuroscience","reference-count":98,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,1,27]],"date-time":"2026-01-27T00:00:00Z","timestamp":1769472000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Medical Research Council","award":["MC_UP_1201\/25"],"award-info":[{"award-number":["MC_UP_1201\/25"]}]},{"name":"Medical Research Council","award":["MC_U105174197"],"award-info":[{"award-number":["MC_U105174197"]}]},{"name":"Medical Research Council","award":["BSF41"],"award-info":[{"award-number":["BSF41"]}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["R01-NS137469"],"award-info":[{"award-number":["R01-NS137469"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["R01-NS110437"],"award-info":[{"award-number":["R01-NS110437"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["RF1-AG071177"],"award-info":[{"award-number":["RF1-AG071177"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["R01-AG080001"],"award-info":[{"award-number":["R01-AG080001"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000893","name":"Simons Foundation","doi-asserted-by":"crossref","award":["529508"],"award-info":[{"award-number":["529508"]}],"id":[{"id":"10.13039\/100000893","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,1,27]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                <jats:p>\n                  The assembly of TAR DNA-binding protein 43 (TDP-43) into amyloid filaments within neurons is a hallmark of multiple neurodegenerative diseases, including motor neuron diseases (MND), frontotemporal dementias (FTD) and limbic-predominant age-related TDP-43 encephalopathy (LATE). These diseases result from the deterioration and loss of neurons, with synaptic dysfunction and neuronal hyperexcitability being prominent early events. Pathogenic mutations in the TDP-43 gene,\n                  <jats:italic>TARDBP<\/jats:italic>\n                  , that promote filament formation have established a causal role for TDP-43 assembly in neurodegenerative diseases. However, the molecular mechanisms underlying filament accumulation and their contribution to neurodegeneration are poorly understood. TDP-43 filaments can propagate between neurons in a prion-like manner, which may underlie the progressive spread and accumulation of TDP-43 pathology in disease. Here, we studied early stages of TDP-43 filament accumulation following internalisation of patient-derived TDP-43 filaments by mouse and human cortical neurons. Using proximity labelling, we identified molecular environments and putative interactions of TDP-43 filaments. We found that TDP-43 filaments accumulated at synapses, particularly in proximity to the presynaptic active zone, which we confirmed in FTD patient brain sections. Electron cryo-tomography (cryo-ET) directly visualised abundant TDP-43 filaments spanning the presynaptic cytoplasm\n                  <jats:italic>in situ<\/jats:italic>\n                  , which contacted synaptic vesicles and the plasma membrane. Functional measurements revealed that the accumulation of TDP-43 filaments led to presynaptic dysfunction and subsequent neuronal hyperexcitability. These findings suggest that synapses are a major early site of TDP-43 filament accumulation, relevant to their propagation, and directly link TDP-43 filament gain of function to synaptic dysfunction.\n                <\/jats:p>","DOI":"10.64898\/2026.01.27.701787","type":"posted-content","created":{"date-parts":[[2026,1,27]],"date-time":"2026-01-27T22:25:13Z","timestamp":1769552713000},"source":"Crossref","is-referenced-by-count":0,"title":["Pathological TDP-43 filaments accumulate at synapses and cause synaptic dysfunction"],"prefix":"10.64898","author":[{"given":"Renren","family":"Chen","sequence":"first","affiliation":[{"name":"MRC Laboratory of Molecular Biology, Cambridge, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Imogen","family":"Stockwell","sequence":"additional","affiliation":[{"name":"MRC Laboratory of Molecular Biology, Cambridge, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jessica 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