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Without adequate B12, homocysteine levels rise, and elevated homocysteine is neurotoxic, potentially causing direct damage to nerve cells and blood vessels that supply nerves

[26] DNA methylation is involved in the functioning of genes and is an essential epigenetic control mechanism in mammals

(as long as the causative factor for B 12 deficiency persists, therapy should be continued) Evidence from animal and human studies shows that B 12 also has neuroprotective and anti-inflammatory properties, 15 and intervention studies in humans have reported beneficial effects of better B 12 status or B 12 therapy in multiple sclerosis, 16 Parkinsons disease, 17 myalgic encephalomyelitis, 18 autism, 19 and (administering very high doses of methylcobalamin) in amyotrophic lateral sclerosis

The core of the 5-Amino-1MQ vs MOTS-c debate lies in their targets

Scientific opinion on dietary reference values for cobalamin (vitamin B12)

The two-year study found that the supplementation improved B-vitamin status, decreased homocysteine concentrations, and reduced risk of total fractures compared to placebo (117)