Get Newsletter
Alzheimer Research Forum - Networking for a Cure Alzheimer Research Forum - Networking for a CureAlzheimer Research Forum - Networking for a Cure
  
What's New HomeContact UsHow to CiteGet NewsletterBecome a MemberLogin          
Papers of the Week
Current Papers
ARF Recommends
Milestone Papers
Search All Papers
Search Comments
News
Research News
Drug News
Conference News
Research
AD Hypotheses
  AlzSWAN
  Current Hypotheses
  Hypothesis Factory
Forums
  Live Discussions
  Virtual Conferences
  Interviews
Enabling Technologies
  Workshops
  Research Tools
Compendia
  AlzGene
  AlzRisk
  Antibodies
  Biomarkers
  Mutations
  Protocols
  Research Models
  Video Gallery
Resources
  Bulletin Boards
  Conference Calendar
  Grants
  Jobs
Early-Onset Familial AD
Overview
Diagnosis/Genetics
Research
News
Profiles
Clinics
Drug Development
Companies
Tutorial
Drugs in Clinical Trials
Disease Management
About Alzheimer's
  FAQs
Diagnosis
  Clinical Guidelines
  Tests
  Brain Banks
Treatment
  Drugs and Therapies
Caregiving
  Patient Care
  Support Directory
  AD Experiences
Community
Member Directory
Researcher Profiles
Institutes and Labs
About the Site
Mission
ARF Team
ARF Awards
Advisory Board
Sponsors
Partnerships
Fan Mail
Support Us
Return to Top
Home: News
News
News Search  
Bile Acid Proves Neuroprotective in Huntington's Model
6 August 2002. A mitochondria-protecting, anti-apoptotic bile acid can reduce neurodegeneration and motor deficits in a mouse model of Huntington's disease, according to a report in the current Proceedings of the National Academy of Science. Noting that the compound has proven safe in other FDA-approved uses, the authors suggest it could be used as a therapy for other neurodegenerative disorders as well.

Coauthor Clifford Steer's molecular gastroenterology laboratory at the University of Minnesota in Minneapolis first discovered the anti-apoptotic properties of tauroursodeoxycholic acid (TUDCA). Subsequent work has shown that TUDCA is an antioxidant and that it inhibits mitochondrial processes that might contribute to neurodegeneration. In the present study, conducted with Walter Low, Dirk Keene, and other neuroscientists at Minnesota, TUDCA was administered to the R6/2 transgenic HD mouse, beginning at 6 weeks of age. Compared to untreated Tg mice, the treated mice showed less striatal atrophy, decreased striatal apoptosis and a reduction in abnormal huntingtin protein aggregates. More importantly, locomotor and sensorimotor deficits were significantly improved in the treated mice.

Also important was the fact that these results were achieved with systemic TUDCA, indicating that the compound can cross the blood/brain barrier. Given that TUDCA is produced endogenously and has shown few side-effects in its current uses in gastroenterologic disease, the authors propose that it could have potential in treating other neurodegenerative disorders that involve mitochondrial dysfunction, including Alzheimer's.-Hakon Heimer

Reference
Keene CD, Rodrigues CMP, Eich T, Chhabra MS, Steer CJ, Low WC. Tauroursodeoxycholic acid, a bile acid, is neuroprotective in a transgenic animal model of Huntington's disease. PNAS. 6 Aug 2002;99(16):10671-6. Abstract <

 
Comments on News and Primary Papers
  Comment by:  M. Flint Beal
Submitted 6 August 2002  |  Permalink Posted 6 August 2002

The recent study demonstrating that tauroursodeoxycholic acid exerts significant therapeutic effects in a transgenic mouse model of Huntington's Disease (HD) is extremely intriguing. This agent was previously demonstrated to stabilize mitochondria and inhibit release of cytochrome-c, which has been linked to apoptotic cell death. This prevents activation of downstream caspases. It is possible that similar mechanisms may play a role in Alzheimer's Disease (AD) pathogenesis. There is substantial evidence showing that a number of markers for apoptotic cell death are increased in AD postmortem brain tissue. There is also substantial evidence for mitochondrial dysfunction in AD. Decreases in cytochrome oxidase activity have been demonstrated both in postmortem as well as in peripheral tissues such as platelets. Reductions in alpha-ketoglutorate dehydrogenase activity are found in both fibroblasts as well as in brain tissue.

There is also a large body of evidence implicating increased oxidative damage in AD. All of these processes may be linked to mitochondrial dysfunction....  Read more

  Submit a Comment on this News Article
Cast your vote and/or make a comment on this news article. 

If you already are a member, please login.
Not sure if you are a member? Search our member database.

*First Name  
*Last Name  
Country or Territory:
*Login Email Address  
*Password    Minimum of 8 characters
*Confirm Password  
Stay signed in?  

I recommend the Primary Papers

Comment:

(If coauthors exist for this comment, please enter their names and email addresses at the end of the comment.)

References:


*Enter the verification code you see in the picture below:


This helps Alzforum prevent automated registrations.

Terms and Conditions of Use:Printable Version

By clicking on the 'I accept' below, you are agreeing to the Terms and Conditions of Use above.
Print this page
Email this page
Alzforum News
Papers of the Week
Text size
Share & Bookmark
ADNI Related Links
ADNI Data at LONI
ADNI Information
DIAN
Foundation for the NIH
AddNeuroMed
neuGRID
Desperately

Antibodies
Cell Lines
Collaborators
Papers
Research Participants
Copyright © 1996-2013 Alzheimer Research Forum Terms of Use How to Cite Privacy Policy Disclaimer Disclosure Copyright
wma logoadadad