Abstract
Evidence for the neuroprotective effects of TUDCA was first shown in experimental or animal models of Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, multiple sclerosis,18 and amyotrophic lateral sclerosis (ALS). These preclinical studies found that TUDCA regulates and inhibits apoptosis; reduces production of reactive oxygen species; protects mitochondria; and acts as a chemical chaperone to stabilize the unfolded protein response.8 Several clinical trials are now underway to evaluate the safety and efficacy of TUDCA in the treatment of neurodegeneration. Data from these trials has shown that TUDCA is safe and potentially effective in ALS, which is now the first neurodegenerative condition to be treated with hydrophilic bile acids. Further evidence is being collected with regard to Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and multiple sclerosis.
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