Protecting the brain from a deadly genetic disease
February 22, 2010 by admin · Leave a Comment
Contact: Kathy Wallis
kwallis3@uwo.ca
519-661-2111 x81136
University of Western Ontario
Huntington’s disease (HD) is a cruel, hereditary condition that leads to severe physical and mental deterioration, psychiatric problems and eventually, death. Currently, there are no treatments to slow down or stop it. HD sufferers are born with the disease although they do not show symptoms until late in life. In a new study published in The Journal of Neuroscience, Stephen Ferguson and Fabiola Ribeiro of Robarts Research Institute at The University of Western Ontario identified a protective pathway in the brain that may explain why HD symptoms take so long to appear. The findings could also lead to new treatments for HD.
Drug shows promise for Huntington’s disease
February 7, 2010 by admin · Leave a Comment
Contact: Mark Michaud
mark_michaud@urmc.rochester.edu
585-273-4790
University of Rochester Medical Center
An early stage clinical trial of the experimental drug dimebon (latrepirdine) in people with Huntington’s disease appears to be safe and may improve cognition. That is the conclusion of a study published today in the Archives of Neurology.
Discovery of mechanism in brain cell injury in Huntington’s offers new treatment approaches
January 26, 2010 by admin · Leave a Comment
Contact: Melissa Ashman
mashman@brain.ubc.ca
604-827-3396
University of British Columbia Read more
UCLA scientists find molecular switch to prevent Huntington’s disease in mice
December 23, 2009 by admin · Leave a Comment
Contact: Elaine Schmidt Haber
ehaber@mednet.ucla.edu
310-794-2272
University of California - Los Angeles Read more
Small changes in protein chemistry play large role in Huntington’s disease
December 23, 2009 by admin · Leave a Comment
Contact: Gregory Roa
greg.roa@nih.gov
301-496-5751
NIH/National Institute of Neurological Disorders and Stroke
In Huntington’s disease, a mutated protein in the body becomes toxic to brain cells. Recent studies have demonstrated that a small region adjacent to the mutated segment plays a major role in the toxicity. Two new studies supported by the National Institutes of Health show that very slight changes to this region can eliminate signs of Huntington’s disease in mice.
Subtle change dramatically reduces pathogenic potential of Huntington’s protein
December 22, 2009 by admin · Leave a Comment
Contact: Cathleen Genova
cgenova@cell.com
617-397-2802
Cell Press
Scientists have identified a key molecular switch that may drive the onset of Huntington’s disease (HD), an incurable neurodegenerative disorder that leads to severe disruptions in muscle coordination and cognitive function. The research, published by Cell Press in the December 24 issue of the journal Neuron, enhances the understanding of HD pathogenesis and may direct new strategies for treating this devastating brain disease.
IKK may act as both inhibitor and promoter of Huntington’s disease
December 20, 2009 by admin · Leave a Comment
Contact: Rita Sullivan
news@rupress.org
212-327-8603
Rockefeller University Press
The kinase IKK phosphorylates the protein mutated in Huntington’s disease to promote its removal and neuron survival, but IKK may be a double-edged sword that increases neurotoxicity in later stages of the disease. The study, led by researchers from the University of California, Irvine, will be published online December 21 in the Journal of Cell Biology (www.jcb.org).
Researchers find potential treatment for Huntington’s disease
November 15, 2009 by admin · Leave a Comment
Investigators at Burnham Institute for Medical Research (Burnham), the University of British Columbia’s Centre for Molecular Medicine and Therapeutics and the University of California, San Diego have found that normal synaptic activity in nerve cells (the electrical activity in the brain that allows nerve cells to communicate with one another) protects the brain from the misfolded proteins associated with Huntington’s disease. In contrast, excessive extrasynaptic activity (aberrant electrical activity in the brain, usually not associated with communication between nerve cells) enhances the misfolded proteins’ deadly effects. Researchers also found that the drug Memantine, which is approved to treat Alzheimer’s disease, successfully treated Huntington’s disease in a mouse model by preserving normal synaptic electrical activity and suppressing excessive extrasynaptic electrical activity. The research was published in the journal Nature Medicine on November 15.
CSHL team solves structure of NMDA receptor unit that could be drug target for neurological diseases
November 12, 2009 by admin · Leave a Comment
A domain of the NR2B subunit of the NMDA receptor is mapped in exquisite detail
Cold Spring Harbor, NY — A team of scientists at Cold Spring Harbor Laboratory (CSHL) reports on Thursday their success in solving the molecular structure of a key portion of a cellular receptor implicated in Alzheimer’s, Parkinson’s, and other serious illnesses.
Caltech researchers show efficacy of gene therapy in mouse models of Huntington’s disease
November 1, 2009 by admin · Leave a Comment
Antibodies against intracellular targets can reduce symptoms, lengthen life span
Pasadena, Calif.Researchers at the California Institute of Technology (Caltech) have shown that a highly specific intrabody (an antibody fragment that works against a target inside a cell) is capable of stalling the development of Huntington’s disease in a variety of mouse models.
