Neuroprotective effects of sodium molybdate in a beta-amyloid-induced rat model of Alzheimer's disease: An In Vivo preclinical study.

BACKGROUND

Molybdenum, as a trace element, exhibits various pharmacological properties, including antioxidant, anti-inflammatory, and free radical-scavenging activities. This study aimed to evaluate the effects of sodium molybdate on neurotoxicity induced by beta-amyloid (Aβ) in adult male Wistar rats.

METHODS

Forty-eight rats were randomly divided into eight groups: Healthy control group, Experimental groups receiving sodium molybdate (0.1, 0.2, and 0.4 mg/kg intragastrically daily), Alzheimer's control group (intrahippocampal injection of Aβ bilaterally), and Alzheimer's experimental groups receiving sodium molybdate (0.1, 0.2, and 0.4 mg/kg intragastrically daily) for 30 consecutive days following Aβ injection. Histopathological changes in the hippocampus were assessed using Hematoxylin and Eosin staining, and amyloid plaques were evaluated via Congo Red staining. The expression levels of GFAP and S100 proteins were investigated by immunohistochemistry, and changes in the expression level of Bax/Bcl2 ratio were evaluated by Real-time PCR in the hippocampus.

FINDINGS: Our results revealed a dose-dependent attenuation of neuronal degeneration, and reduced amyloid plaque formation in the Alzheimer's experimental groups following sodium molybdate administration. Treatment with sodium molybdate at doses of 0.2 and 0.4 mg/kg significantly reduced the levels of both S100 and GFAP proteins (P < 0.05 and P < 0.001 respectively) compared to the Alzheimer's control group. Furthermore, sodium molybdate administration at a dose of 0.1 mg/kg significantly reduced the Bax/Bcl2 expression ratio (P < 0.05), with greater reductions observed at 0.2 and 0.4 mg/kg doses (P < 0.01).

CONCLUSION

The results of this study suggest that sodium molybdate may exert protective effects against neurological disorders caused by Aβ in a rat model of Alzheimer's disease.