Modeling how vitamin B12 affects neuroinflammation, muscle atrophy and neurodegeneration.
Compute the Truth™ YourselfEach graph compares the matched normal-model reference with the ALS model condition at 0 nM vitamin B12, followed by increasing vitamin B12 inputs. All vitamin B12 inputs and biomarker outputs are shown in nM.
Modeled effects on two inflammatory signaling molecules associated with immune activity in the nervous system.
TNF-α is a pro-inflammatory cytokine associated with inflammatory signaling in the nervous system.
The modeled TNF-α output decreases as vitamin B12 input increases, from approximately 18.5 nM in the ALS condition to 12.6 nM at 17,000 nM B12. The output remains far above the matched normal-model reference of 0.00012 nM.
IL-6 participates in inflammatory communication and changes with immune activation.
The modeled IL-6 output decreases progressively with vitamin B12 input, from approximately 0.0315 nM in the ALS condition to 0.0221 nM at 17,000 nM B12. It does not reach the approximate normal-model reference shown in the supplied deck.
Modeled effects on extracellular-matrix outputs and MuRF1, a regulator of muscle protein breakdown.
Collagen is part of the extracellular matrix that supports muscle structure. Excess remodeling or accumulation may accompany muscle injury and fibrosis, but interpretation depends on the collagen species and tissue compartment.
The modeled collagen output falls with increasing vitamin B12 input. The slide does not identify the collagen type, so this result should be read as a model-specific collagen output rather than a clinical collagen measurement.
Fibronectin organizes extracellular matrix and cell-matrix interactions. Changes can reflect tissue remodeling rather than a direct measure of muscle strength.
The modeled fibronectin output decreases from approximately 0.755 nM in the ALS condition to 0.109 nM at the highest B12 input. It remains above the approximate normal-model reference.
MuRF1 is a muscle-specific ubiquitin ligase involved in degradation of contractile proteins during atrophy.
The modeled MuRF1 output decreases as vitamin B12 input rises, from approximately 249 nM in the ALS condition to 48 nM at 17,000 nM B12. The result moves toward, but remains well above, the matched normal-model reference.
Modeled effects on ER-stress signaling and an autophagy-associated readout.
CHOP is induced during prolonged endoplasmic-reticulum stress and can participate in stress-associated cell-death signaling.
The modeled CHOP output decreases sharply with vitamin B12 input, from approximately 79.3 nM in the ALS condition to 10.1 nM at the highest input. It remains above the normal-model reference.
LC3-II marks autophagosome-associated LC3, but a single LC3-II concentration cannot determine whether autophagic flux has increased or decreased.
The model predicts lower LC3-II output as vitamin B12 input rises. This movement toward the normal-model value should be interpreted as a modeled LC3-II change, not by itself as proof that autophagy has normalized.
A 16-week randomized clinical trial in Japanese patients with early-stage ALS and moderate progression reported slower functional decline with ultrahigh-dose methylcobalamin than with placebo.
This clinical regimen does not establish equivalence with the model inputs shown on this page.
Oki et al., 2022 →Higher circulating vitamin B12 was associated with lower IL-6 and C-reactive protein in humans and with lower IL-6 in mice.
Association does not establish that vitamin B12 directly controls every inflammatory pathway modeled here.
Domínguez-López et al., 2024 →LC3-II at one time point does not by itself measure autophagic flux. Interpretation requires comparison under conditions that reveal lysosomal delivery and turnover.
The LC3-II graph therefore reports a model output rather than a clinical conclusion about restored autophagy.
Mizushima & Yoshimori, 2007 →These modeled results do not establish a clinical dose, treatment recommendation or individual outcome. Input concentrations are retained exactly as labeled in the supplied source deck.
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