Study finds clue in preventing Alzheimer's.
Alzheimer's Donation
Donate Online Now
.
NEW YORK, July 6 (UPI) -- Researchers said Thursday that the enzyme IDE -- at low levels in Alzheimer's patients -- may be a key to preventing the illness.
Researchers at the Neuroinflammation Research Center at Mount Sinai School of Medicine in New York set out to test the theory that increasing the amount of IDE in the body with synthetic enzymes as soon as levels start to drop could prevent the onset of Alzheimer's disease. The team saw that IDE levels were low in the memory-crucial hippocampus and entorhinal cortex of the brains of people with mild cognitive impairment, often a precursor to Alzheimer's. IDE breaks down beta-amyloid peptides, which cause amyloid brain plaques if their production is unchecked.
The team hypothesized that low IDE was responsible for the formation of these plaques. To test their theory, they measured beta-amyloid and IDE levels in the postmortem brain tissue of 46 elderly subjects and found that low IDE activity was indeed associated with elevated beta-amyloid peptides in both the hippocampus and entorhinal cortex.
The researchers said they will next determine how soon low IDE levels can be detected in the blood, and whether boosting these levels pharmacologically will prevent the formation of amyloid brain plaques and stop Alzheimer's disease before it begins.
Results of the study can be found in the June 10 online issue of Neurobiology of Aging.
Researchers at the Neuroinflammation Research Center at Mount Sinai School of Medicine in New York set out to test the theory that increasing the amount of IDE in the body with synthetic enzymes as soon as levels start to drop could prevent the onset of Alzheimer's disease. The team saw that IDE levels were low in the memory-crucial hippocampus and entorhinal cortex of the brains of people with mild cognitive impairment, often a precursor to Alzheimer's. IDE breaks down beta-amyloid peptides, which cause amyloid brain plaques if their production is unchecked.
The team hypothesized that low IDE was responsible for the formation of these plaques. To test their theory, they measured beta-amyloid and IDE levels in the postmortem brain tissue of 46 elderly subjects and found that low IDE activity was indeed associated with elevated beta-amyloid peptides in both the hippocampus and entorhinal cortex.
The researchers said they will next determine how soon low IDE levels can be detected in the blood, and whether boosting these levels pharmacologically will prevent the formation of amyloid brain plaques and stop Alzheimer's disease before it begins.
Results of the study can be found in the June 10 online issue of Neurobiology of Aging.
posted by Valery Yermalitsky at
5:48 AM
0 Comments:
Post a Comment
Subscribe to Post Comments [Atom]
<< Home