Journal
EXPERIMENTAL NEUROLOGY
Volume 171, Issue 2, Pages 351-360Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1006/exnr.2001.7755
Keywords
Huntington's disease; 3-nitropropionic acid; bile acid; tauroursodeoxycholic acid; mitochondria; apoptosis; striatum; neuroprotection
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Funding
- NIMH NIH HHS [5F30MH12157-02] Funding Source: Medline
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There is currently no effective treatment for Huntington's disease (HD), a progressive, fatal, neurodegenerative disorder characterized by motor and cognitive deterioration. It is well established that HD is associated with perturbation of mitochondrial energy metabolism. Tauroursodeoxycholic acid (TUDCA), a naturally occurring bile acid, can stabilize the mitochondrial membrane, inhibit the mitochondrial permeability transition, decrease free radical formation, and derail apoptotic pathways. Here we report that TUDCA significantly reduced 3-nitropropionic acid (3NP)-mediated striatal neuronal cell death in cell culture. In addition, rats treated with TUDCA exhibited an 80% reduction in apoptosis and in lesion volumes associated with 3-NP administration. Moreover, rats which received a combination of TUDCA + 3-NP exhibited sensorimotor and cognitive task performance that was indistinguishable from that of controls, and this effect persisted at least 6 months. Bile acids have traditionally been used as therapeutic agents for certain liver diseases. This is the first demonstration, however, that a bile acid can be delivered to the brain and function as a neuroprotectant and thus may offer potential therapeutic benefit in the treatment of certain neurodegenerative diseases. (C) 2001 Academic Press.
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