With the exception of greater solubility, and somewhat different pharmacokinetics, TUDCA and UDCA, are essentially identical molecules that both have the unique ability to increase cell survival and inhibit programmed cell death, or apoptosis. The protective mechanisms of T/UDCA have been studied in a wide range of cell types and animal models of human disease. T/ UDCA is a strong inhibitor of apoptosis by interfering early on with the mitochondrial pathway of cell death and associated processes such as ROS and reducing endoplasmic reticulum stress. T/UDCA serves as a neuroprotectant against acute injuries such as stroke, as well as chronic neurodegenerative diseases including AD, PD, and HD. It protects against cell death in transgenic mouse models of retinitis pigmentosa, ameliorates the insulin resistance associated with obesity, inhibits ER stress associated with type II diabetes, and is approved in South Korea for the treatment of patients with amyotrophic lateral sclerosis.82 It has been reported to be effective in a phase II clinical study for the treatment of transthyretin amyloidosis in combination with doxycycline.83 T/UDCA has been shown to be effective in animal models of spinal cord injury,84 head trauma, glaucoma, acute renal failure, pancreatitis, metabolic syndrome, psoriasis,85,86 myocardial infarction, neuropathic pain,87 ischemia reperfusion syndromes, GI disorders, and diabetic retinopathy in addition to the obvious liver-related disorders. Obese patients seem to benefit from T/UDCA via the inhibition of ER stress and UPR dysfunction. Patients with macular degeneration, hair loss and early onset of aging may benefit from the remarkable properties of T/UDCA.