[4] In Canada and the United States, ursodoxicoltaurine, in combination with sodium phenylbutyrate, was indicated for the treatment of amyotrophic lateral sclerosis (ALS).

If the mitochondria are distressed, they release cytochrome C (cyC) and calcium which activate caspases to propagate a cascade of cellular mechanisms to cause apoptosis.

[9] Tauroursodeoxycholic acid also acts as a chemical chaperone to help maintain the stability and correct folding of proteins.

[10] Ursodoxicoltaurine has been shown to reduce apoptosis and to have protective effects in neurodegenerative diseases and the eye, particularly for retinal degenerative disorders.

[12] Another study, from the Department of Ophthalmology at Johns Hopkins University, in Baltimore, Maryland, saw similar effects in two components of bile, bilirubin and ursodoxicoltaurine, in relation to RP.

In the albino mice models, intraperitoneal injections of bilirubin or ursodoxicoltaurine were given prior to prolonged light exposure.

Both treatments had positive effects on the health of the mouse retina, including a reduced accumulation of superoxide radicals, rod cell death, and disruption of cone inner and outer segments.

[13] A study done at the Department of Ophthalmology at Seoul National University College of Medicine examined the effects of ursodoxicoltaurine and UDCA on laser-treated choroids of rat models.

The amplitude of the a- and b- waves were considerably higher in ursodoxicoltaurine treated rats, compared to the control group.

The neuroprotective effects of ursodoxicoltaurine are not only preserving retinal morphology and function, but also its synaptic contacts, a potentially useful aspect in delaying RP.