The study "Decreased Brain Levels of Vitamin B12 in Aging, Autism, and Schizophrenia" investigates the relationship between brain vitamin B12 levels and aging, autism, and schizophrenia, focusing on the specific roles of methylcobalamin (MeCbl) and adenosylcobalamin (AdoCbl). The study presents novel insights into the decline of brain B12 levels and its implications for neurodevelopmental and neuropsychiatric disorders.
Key Findings
Vitamin B12 Levels Across the Lifespan
- Age-Dependent Decline: Total B12 levels in the frontal cortex decreased by 2.7-fold in individuals aged 61–80 years compared to those aged 0–20 years. MeCbl showed the most significant decline, dropping 12.4-fold (p < 0.0001).
- Stability in Serum B12: Unlike the brain, serum B12 levels remain relatively stable with age, indicating distinct regulatory mechanisms in the brain.
Vitamin B12 in Autism and Schizophrenia
- Autism:
- Total B12 levels were 3.1-fold lower in autistic subjects compared to age-matched controls (3.1 vs. 8.9 pmol/mg protein; p < 0.001).
- MeCbl levels were over 3-fold lower, correlating with decreased methionine synthase (MS) activity (p < 0.05).
- Schizophrenia:
- Total B12 levels were 3.3-fold lower in schizophrenic individuals (2.2 vs. 7.3 pmol/mg protein; p < 0.001).
- Both MeCbl and AdoCbl levels were significantly reduced (p < 0.01).
Metabolic Implications
- Methionine Cycle:
- Aging and autism were associated with lower methionine and S-adenosylmethionine (SAM) levels, and an impaired SAM-to-S-adenosylhomocysteine (SAH) ratio, indicating reduced methylation potential.
- Oxidative Stress:
- Glutathione (GSH) levels were not significantly different in the frontal cortex of autistic individuals but were reduced in schizophrenia and aging.
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Methodology
Study Design
- Participants:
- 43 control subjects aged 0–80 years.
- 12 autistic individuals (4–9 years).
- 9 schizophrenic individuals (36–49 years).
- Techniques:
- High-performance liquid chromatography (HPLC) was used to measure B12 species and related metabolites.
- Methionine synthase activity was assessed under endogenous and supplemented conditions.
Statistical Analysis
- Results were expressed as mean ± SEM, with statistical significance set at p < 0.05.
- Correlations were evaluated using Pearson's correlation coefficient.
Discussion
Age-Related Changes
- The decline in MeCbl levels is quasi-linear across the lifespan (r² = 0.61). This reduction is associated with diminished methylation potential and impaired epigenetic regulation.
Autism and Schizophrenia
- Both disorders exhibit premature declines in brain B12 levels, resembling the patterns observed in elderly controls. These changes suggest a shared mechanism involving impaired methylation and oxidative stress.
Implications for Treatment
- B12 supplementation, particularly with active forms (MeCbl and AdoCbl), may mitigate deficits in methylation and oxidative stress. The effectiveness of supplementation depends on adequate transport mechanisms and reducing factors like GSH.
Conclusion
This study highlights the critical role of vitamin B12 in maintaining brain function across the lifespan. The findings underscore the need for further research into B12 supplementation as a potential therapeutic strategy for aging, autism, and schizophrenia.
For full details, refer to the original article: https://pubmed.ncbi.nlm.nih.gov/26799654/