Further analysis with AI’s help via Perplexity.ai, gave the following more hopeful information:
Theoretical Risk vs. Empirical Safety:
While in vitro data suggests DMSO could hypothetically worsen α-synuclein pathology, the in vivo mouse study found no evidence of this. Until human data exists, the mouse model provides the best evidence for safety.
Oral DMSO did not induce alpha-synuclein abnormalities in mice: One study showed that oral DMSO treatment did not induce observable alpha-synuclein abnormalities or affect neuronal survival in mice. I believe this is much more important, since the study is based on an animal model and not merely on a test-tube or petri-dish study.
· Theoretical Risk vs. Empirical Safety:
While in vitro data suggests DMSO could hypothetically worsen α-synuclein pathology, the in vivo mouse study found no evidence of this.
· Limitations of In Vitro Models:
Isolated cells lack:
· Protein clearance pathways (ubiquitin-proteasome, autophagy).
· Neuroprotective mechanisms (e.g., chaperone proteins, antioxidant enzymes).
· Tissue-level interactions.
· Cautious Optimism:
DMSO’s antioxidant, anti-inflammatory, and membrane-stabilizing properties could theoretically benefit LBD. The absence of toxicity in mice justifies further research but not unsupervised use.
Biological Relevance:
Mouse models account for systemic factors (absorption, distribution, metabolism) absent in cell cultures. The absence of pathology in vivo suggests compensatory mechanisms may mitigate DMSO’s pro-aggregation effects observed in vitro.
Dose and Route Consistency:
The oral DMSO doses tested (1–3 g/kg/day) exceed typical human therapeutic doses (0.1–0.5 g/kg/day), yet still showed no adverse effects. This supports potential safety in physiological contexts.
In Summary, prioritization of the in vivo mouse data is well-founded: the absence of α-synuclein pathology or neurodegeneration after oral DMSO administration in mice significantly outweighs concerns from in vitro studies. This suggests that DMSO’s aggregation-promoting effects in simplified systems may not translate to living organisms. However, human data remains absent, and DMSO’s efficacy for LBD is unproven. Rigorous clinical trials are needed before endorsing its use.
Are any of you readers able to add to or further illuminate the above information about DMSO’s effectiveness in treating Lewy Body Dementia?