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Occupational and environmental exposure to vanadium is connected to a neurological syndrome that includes psychiatric symptoms, cognitive decline, and neurodegeneration. In this study, we hypothesized that prolonged vanadium exposure may be a potential risk factor for Alzheimer's and Parkinson's diseases. A total of 72 male BALB\/c mice, each 4\u2009weeks' old, were used. Vanadium\u2010treated groups received intraperitoneal injections of 3\u2009mg\/kg body weight of vanadium three times a week for 6, 12, or 18\u2009months. The control group received sterile water while the withdrawal group were given vanadium injection for 3\u2009months, followed by withdrawal of the metal, but treatment with sterile water only, and were sacrificed at 3\u2010, 9\u2010, or 15\u2010months post vanadium exposure. Sagittal sections of brain paraffin\u2010embedded tissue were prepared and analyzed using immunofluorescence to study the immunoreactivity and cellular localization of \u03b1\u2010synuclein (\u03b1\u2010syn), amyloid\u2010\u03b2 (A\u03b2), and tau proteins. Our findings revealed pathological aggregation of these proteins in the frontoparietal cortices and the dorsal CA1 and CA3 regions. Double immunolabeling with glial cells and neurons showed neuronal degeneration, functional gliosis, and activation of astrocytes and microglia at sites of \u03b1\u2010synuclein immunoreactivity. We observed increased immunoreactivity of phosphorylated nuclei tau both in the parietal cortices and corpus callosum white matter while we observed intraneuronal accumulation of A\u03b2 deposits in the cortex and dorsal hippocampal regions in vanadium treated brains. These cellular changes and proteinopathies, although persisting, were significantly attenuated after vanadium withdrawal. Our findings show that prolonged vanadium exposure promotes abnormal accumulation of neurodegeneration\u2010associated proteins (\u03b1\u2010syn, Tau, and A\u03b2) in the brain, which is further exacerbated by aging in the context of extended exposure to the metal.\n                    <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                      <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/jnc70082-fig-0011-m.png\">\n                        <jats:alt-text>image<\/jats:alt-text>\n                      <\/jats:graphic>\n                    <\/jats:boxed-text>\n                  <\/jats:p>","DOI":"10.1111\/jnc.70082","type":"journal-article","created":{"date-parts":[[2025,5,16]],"date-time":"2025-05-16T06:44:08Z","timestamp":1747377848000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Chronic Vanadium Exposure Promotes Aggregation of Alpha\u2010Synuclein, Tau and Amyloid Beta in Mouse Brain"],"prefix":"10.1111","volume":"169","author":[{"given":"O. 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