A bile acid protects against motor and cognitive deficits and reduces striatal degeneration in the 3-nitropropionic acid model of Huntington's disease
In: Symposium Vasopressin: Integrative and Cellular Mechanisms of Release and ActionsExperimental neurology (Print) 171(2):351-360; Jg. 171 (2001) 2, S. 351-360
Konferenz
- print, 63 ref
Zugriff:
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 (3-NP)-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.
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A bile acid protects against motor and cognitive deficits and reduces striatal degeneration in the 3-nitropropionic acid model of Huntington's disease
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Autor/in / Beteiligte Person: | KEENE, C. Dirk ; RODRIGUES, Cecilia M. P ; EICH, Tacjana ; LINEHAN-STIEERS, Cheryle ; ABT, Anna ; KREN, Betsy T ; STEER, Clifford J ; LOW, Walter C |
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Quelle: | Symposium Vasopressin: Integrative and Cellular Mechanisms of Release and ActionsExperimental neurology (Print) 171(2):351-360; Jg. 171 (2001) 2, S. 351-360 |
Veröffentlichung: | Amsterdam: Elsevier, 2001 |
Medientyp: | Konferenz |
Umfang: | print, 63 ref |
ISSN: | 0014-4886 (print) |
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