ArticleFrontiers in aging neuroscience2026
Atherosclerotic-dose TMAO accentuates redox imbalances and motor dysfunctions in a MPTP mouse model of Parkinson's disease.
Article in Frontiers in aging neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Parkinson's Disease (PD) involves the loss of dopaminergic neurons and the formation of Lewy bodies consisting of alpha-synuclein (αSin) aggregates. Trimethylamine N-oxide (TMAO), a gut microbiota metabolite, has emerged as a molecule of interest due to pro-inflammatory, pro-oxidative, and neurodegenerative effects. We aim to assess whether lower doses of TMAO (40 mg/kg bw, gavage, once daily, day 0-42), as those used in atherosclerosis experimental models, can exacerbate oxidative stress, neuroinflammation, motor dysfunction, and neurodegeneration in a semi-acute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) PD model (30 mg/kg bw MPTP, intraperitoneal, once daily, day 20-24). Motor behavioral testing functionally validated the model, with MPTP impairing performance across Rotarod latency time (
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