Evaluation of neuroprotective effects of cobalamin (vitamin B12) in Parkinson's disease - Investigation of molecular mechanisms

‌Background & objectives: Parkinson's disease is one of the most common neurodegenerative diseases that its prevalence has increased in recent years. Although many efforts have been made to treat this disease, so far, no therapeutic approach has been found that can stop the destruction of dopaminergic cells in the substantia nigra. The aim of the present study was to investigate the effect of vitamin B12 administration on Parkinson's female mice and their embryos. Materials & Methods: Induction of Parkinson's disease in female mice was performed using rotenone and vitamin B12 administration was started one hour after Parkinson's induction and was performed for 14 days. On day 14, the animals underwent apomorphine-induced rotation testing, and then half of the animals were killed according to ethical protocols, and cerebellar tissue homogenates were prepared. The other half of the animals were allowed to mate with male mice and kept in separate cages after their pregnancy was confirmed. The embryos were isolated on the 21st day of gestation and their cerebellar tissue homogenates were also prepared. Cell viability was measured by MTT method and apoptosis and necrosis were measured by flow cytometry. Also, the expression of bax and bcl-2 genes was measured using RT-PCR. Data analysis was performed in GraphPad Prism V.8 software. Results: Survival, apoptosis and necrosis of cerebellar neurons in female mice and fetuses from Parkinson's mice were significantly affected by vitamin B12 administration and an increase in survival and a decrease in apoptosis and necrosis of cerebellar neurons were observed with vitamin B12 administration. Also, decreased bax gene expression and increased bcl-2 expression were observed in the cerebellar neurons of Parkinson's animals receiving vitamin B12. Conclusion: Vitamin B12 has neuroprotective effects in Parkinson's disease and can be considered as a treatment option.