Objective: In this study, we hypothesized that prolonged vanadium exposure may be a potential risk factor for Alzheimer’s and Parkinson’s diseases.
Background: The interaction between toxic environmental metals or metalloids and brain proteins can lead to pathological aggregation and the formation of toxic oligomer which are hallmark features of many neurodegenerative disorders. Vanadium, a widespread environmental and occupational contaminant, has been linked to neurological impairments marked by behavioral disturbances, cognitive decline, and progressive neuronal damage.
Method: A total of seventy-two male BALB/c mice, aged four weeks, were utilized. Experimental groups received intraperitoneal doses of 3 mg/kg body weight of vanadium three times per week over 6, 12, or 18 months, while controls were given sterile water. The withdrawal groups received vanadium for 3 months followed by sterile water only and were sacrificed at 3, 9, or 15 months after exposure. Cognitive performance was evaluated at 6, 12, and 18 months using the Morris water maze. Paraffin-embedded sagittal brain sections were analyzed through immunofluorescence to determine the expression and localization of α-synuclein (α-syn), amyloid-β (Aβ), and tau proteins.
Results: Vanadium-exposed mice exhibited significant impairments in memory across the 6–18-month exposure period, with notable recovery observed only 9 months after withdrawal of vanadium treatment. Pathological aggregation of α-syn, Aβ, and tau was detected in the frontoparietal cortices and hippocampal CA1 and CA3 regions. Double immuno-labeling with neuronal and glial markers revealed neuronal degeneration, reactive gliosis, and activation of astrocytes and microglia in α-syn–positive regions. Increased phosphorylated tau immunoreactivity was observed in the parietal cortex and corpus callosum, alongside intraneuronal Aβ accumulation in cortical and hippocampal areas.
Conclusion: Our findings show that prolonged vanadium exposure promotes cognitive impairment and abnormal accumulation of neurodegeneration-associated proteins (α-syn, Tau, and Aβ) in the brain, which is further exacerbated by aging in the context of extended exposure to the metal.
To cite this abstract in AMA style:
O. Folarin, F. Olopade, T. Gilbert, A. Ladagu, P. Inês, O. Mustapha, L. Zethan, J. Olopade, T. Outeiro. Chronic Vanadium Exposure Promotes Memory Impairment and Aggregation of Alpha-Synuclein, Tau and Amyloid Beta in Mouse Brain [abstract]. Mov Disord. 2026; 41 (suppl 1). https://www.mdsabstracts.org/abstract/chronic-vanadium-exposure-promotes-memory-impairment-and-aggregation-of-alpha-synuclein-tau-and-amyloid-beta-in-mouse-brain/. Accessed October 1, 2026.« Back to 2026 International Congress
MDS Abstracts - https://www.mdsabstracts.org/abstract/chronic-vanadium-exposure-promotes-memory-impairment-and-aggregation-of-alpha-synuclein-tau-and-amyloid-beta-in-mouse-brain/