Scientists have found a way to delay the onset of Huntington's  disease and slow its progress in mice by targeting an enzyme that  is believed to trigger cell death.  

The finding, published in Thursday's issue of the journal  Nature, is a promising lead for drug researchers working to extend  the lives of Huntington's sufferers.  

``I think this is important and exciting. This is the first  demonstration of a drug that can slow the progress of HD in an  animal model,'' said Dr. Christopher Ross, a Johns Hopkins Medical  School professor and a scientific adviser to the Huntington's  Disease Society of America. ``It says this goal of slowing progress  probably can be accomplished.''  

Huntington's has been linked to enzymes called caspases, which  cause brain cells to die slowly.  

In the new study, scientists from Harvard University's Brigham  and Women's Hospital blocked a particular caspase in mice that had  been genetically engineered to contract the disease. These mice  developed Huntington's symptoms about 10 percent later in life and  lived about 20 percent longer.  

Caspase-1 apparently plays a role in the cell death that marks  Huntington's, which usually kills sufferers within 15 to 20 years.  How the enzyme works is unclear, but scientists think that it  slices up the so-called huntingtin gene, and that the fragments  then kill the cell.  

The Harvard researchers slowed that process by breeding mice  with a mutant protein that counteracts caspase-1.  

The mice showed Huntington's symptoms _ walking trouble, weight  loss and seizures _ after 84 days, on average, compared with 77  days in the other mice. The mice with the caspase blocker lived an  average of 121 days, compared with 101 days for the other mice.  

``If one drug can do this, hopefully, in the future, you can  find others,'' said one of the researchers, Dr. Robert M.  Friedlander.  

Huntington's, which killed folk singer Woody Guthrie, afflicts  30,000 Americans.  

What is exciting, Friedlander said, is that the same mechanism  at work in this study may be applied to research on brain injuries  and illnesses such as Lou Gehrig's disease and Parkinson's.  

``Caspase inhibition may turn out to be the magic bullet against  neurodegenerative disease,'' University of Munich biochemist  Christian Haass said in an accompanying editorial.