Vitamin B12 (cobalamin) plays a crucial role in neurodevelopment, particularly during pregnancy and early childhood. It is essential for DNA synthesis, red blood cell formation, and nervous system function. Maternal B12 levels are particularly important, as they influence fetal brain development. Inadequate maternal intake during pregnancy may lead to altered neurodevelopmental trajectories and increase the risk of ASD. Postnatally, insufficient dietary cobalamin in infants and young children could further contribute to cognitive and behavioral impairments. One potential mechanism linking low B12 levels to ASD involves its role in the gut microbiota balance. Dysbiosis, commonly observed in individuals with ASD, is associated with increased gut permeability, low-grade inflammation, and disruptions in the gut–brain axis, all of which may contribute to ASD symptoms. Additionally, B12 is essential for neurotransmitter metabolism, particularly in the synthesis of serotonin and dopamine, which regulate mood, cognition, and behavior. Cobalamin also plays a key role in neuronal myelination, which ensures efficient signal transmission in the nervous system. Disruptions in these processes could underlie some of the cognitive and behavioral features associated with ASD. Despite growing evidence, the link between B12 and ASD remains inconclusive due to inconsistent findings across studies. Research suggests that B12 levels may serve as a potential biomarker for disease progression and treatment response. However, many studies rely on single-time-point measurements, failing to account for individual variability, genetic predispositions, dietary intake, and environmental factors, all of which can influence B12 levels and ASD risk. Further longitudinal studies are needed to clarify this relationship.

Vitamin D₃ plays a pivotal role not only in bone health but also in the functioning of the nervous system, particularly in the context of age-related neurodegenerative diseases such as Alzheimer’s disease, multiple sclerosis, and Parkinson’s disease. Vitamin D₃ deficiency has been associated with cognitive decline, heightened inflammation, and shortened leukocyte telomere length, which may contribute to accelerated cellular aging. Therapeutic interventions involving vitamin D₃ have been reported in selected clinical studies and meta-analyses to potentially enhance cognitive function, decrease amyloid β biomarkers, and prolong telomere length, although heterogeneity remains across study designs and populations. Furthermore, vitamin D₃ has been shown to influence the expression of genes implicated in DNA repair and oxidative stress response, including NRF2, OGG1, MYH, and MTH1. This narrative review synthesizes current knowledge on the molecular mechanisms of vitamin D₃ action in the context of neuroprotection and discusses potential directions for future research, including its possible therapeutic applications in neurodegenerative diseases.

Vitamin B12 (cobalamin) is essential for neurodevelopment, particularly during pregnancy and early childhood. Its deficiency has been implicated in neurological disorders, but also autism spectrum disorder (ASD). Maternal B12 levels influence fetal brain development, and inadequate intake may increase ASD risk. Postnatally, insufficient cobalamin in a child’s diet could further impact neurodevelopment. One mechanism linking B12 deficiency to ASD involves its role in gut microbiota balance. Dysbiosis, common in ASD, is associated with low-grade inflammation and gut-brain axis disruptions. Additionally, B12 is crucial for neurotransmitter metabolism, including serotonin and dopamine synthesis, and for neuronal myelination—both essential for cognitive and behavioral function. Despite emerging evidence, the link between B12 and ASD remains inconclusive due to inconsistent findings. Research suggests B12 may serve as a biomarker for disease progression and treatment response. However, most studies rely on single-time-point measurements, failing to account for individual variability and external influences such as diet and environment. Longitudinal studies are needed to clarify whether early B12 supplementation could mitigate ASD symptoms. Identifying children at risk of deficiency and promoting maternal and early-life nutrition may aid in prevention and intervention.