The role of group B vitamins in neuroprotection

The incidence of cognitive impairment and dementia increases with aging, so it is of much interest to identify and target the risk factors, with the aim of slowing or prevent the cognitive impairment age-related. Numerous studies correlate the group B vitamins shortage to phenomena involved in Alzheimer disease pathogenesis and other neurodegenerative diseases. In literature, we find many studies demonstrating the effect of B vitamins administration in slowing down the cerebral atrophy and cognitive impairment.

Group B vitamins exert neuroprotective effect: as shown in the figure, they protect the neuronal death in hippocampal cultures under stress (Bvit), significantly reducing the amoun of dead cells, compared to the non-treated culture (saline) (Rabie et al., 2010).

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The same effect is observed when neuronal cells are deprived of oxygen and glucose: the B vitamins pre-treatment reduces the apoptotic rate, similar to the healthy control (Li et al., 2019).

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Group B vitamins exert neurotrophic effect: as shown in the figure, in rats receiving diet enriched with B vitamins we observe a significant increase in BDNF expression; BDNF promotes neuronal survival, their maintenance and neurogenesis (Jadavji et al., 2017).

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These observations were confirmed in a clinical study by Douaud et al. (2013). As shown in the figure, the administration od group B vitamins reduces the cerebral atrophy in elderly with initial cognitive impairment, in particular in those areas affected by Alzheimer disease.

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The neuroprotective role of group B vitamins is related to their role as cofactors in homocysteine metabolism: high concentration of this compound are associated to higher risks to be affected by dementia, Alzheimer disease and other cognitive impairments; moreover, also in healthy elderlies higher levels of homocysteine are recorded, associated to cerebral atrophy. So, group B vitamins represent an interesting therapeutic strategy, based on many scientific researches, thanks to their role in homocysteine metabolism.


Douaud, G., Refsum, H., de Jager, C. A., Jacoby, R., Nichols, T. E., Smith, S. M., & Smith, A. D. (2013). Preventing Alzheimer’s disease-related gray matter atrophy by B-vitamin treatment. Proceedings of the National Academy of Sciences, 110(23), 9523-9528.

Jadavji, N. M., Emmerson, J. T., MacFarlane, A. J., Willmore, W. G., & Smith, P. D. (2017). B-vitamin and choline supplementation increases neuroplasticity and recovery after stroke. Neurobiology of disease, 103, 89-100.

Li, E. Y., Zhao, P. J., Jian, J., Yin, B. Q., Sun, Z. Y., Xu, C. X., … & Wu, H. (2019). Vitamin B1 and B12 mitigates neuron apoptosis in cerebral palsy by augmenting BDNF expression through MALAT1/miR-1 axis. Cell cycle, 18(21), 2849-2859.

Rabie, T., Mühlhofer, W., Bruckner, T., Schwab, A., Bauer, A. T., Zimmermann, M., … & Schenkel, J. (2010). Transient protective effect of B-vitamins in experimental epilepsy in the mouse brain. Journal of molecular neuroscience, 41(1), 74-79.

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