A way to reduce amyloid beta deposition.
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he pathological embrace between two proteins, apolipoprotein E (apo E) and amyloid, plays a key role in the development of Alzheimer's disease by triggering the formation of neuron-killing plaques of amyloid beta protein.
The NYU scientists have now devised a way to reduce amyloid beta deposition by interfering with the deadly embrace of these proteins thereby reducing or preventing the aggregation of amyloid beta.
Amyloid beta deposits are one of the defining characteristics of Alzheimer's disease. Although scientists still aren't sure whether plaques are the initial trigger for the disease or are a consequence of it, the clumps can appear years before the onset of clinical symptoms. By the time dementia emerges, the plaques litter the brain.
Apo E acts as a sort of biological chaperone, ferrying cholesterol and fats around the brain. Deprived of its biochemical chaperone, amyloid won't form deadly plaques. The researchers reported a nearly 50 percent reduction in the aggregation of toxic amyloid protein in the brains of mice. In a series of experiments that followed, the researchers noted that the peptide reduced the amount of plaque in the brain and the amount of amyloid in the brain's blood vessels. It also did not cause any apparent inflammation or leaks in blood vessels in the animals' brains.
Finally, another set of experiments showed that the treated mice did not exhibit any memory decline when they were put into a radial arm maze, which evaluates working memory based on the animals' behavior.
The NYU researchers said they were encouraged that their synthetic peptide did not appear to cause inflammation or bleeding in the brains of the animals tested, and that the next step was transforming it into an agent that could be used clinically. "In order for a peptide like this to be used in humans it would have to be taken for many years, much like statin medications for cholesterol. Our ongoing research is now focusing on transforming the peptide used in the study into an agent that could be used clinically. It would have to be taken for a very long period of time without causing toxicity," Dr. Sadowski.
The study is published in the December 5, 2006, issue of the PNAS.
Alzheimer's Donation
Donate Online Now
.
he pathological embrace between two proteins, apolipoprotein E (apo E) and amyloid, plays a key role in the development of Alzheimer's disease by triggering the formation of neuron-killing plaques of amyloid beta protein.
The NYU scientists have now devised a way to reduce amyloid beta deposition by interfering with the deadly embrace of these proteins thereby reducing or preventing the aggregation of amyloid beta.
Amyloid beta deposits are one of the defining characteristics of Alzheimer's disease. Although scientists still aren't sure whether plaques are the initial trigger for the disease or are a consequence of it, the clumps can appear years before the onset of clinical symptoms. By the time dementia emerges, the plaques litter the brain.
Apo E acts as a sort of biological chaperone, ferrying cholesterol and fats around the brain. Deprived of its biochemical chaperone, amyloid won't form deadly plaques. The researchers reported a nearly 50 percent reduction in the aggregation of toxic amyloid protein in the brains of mice. In a series of experiments that followed, the researchers noted that the peptide reduced the amount of plaque in the brain and the amount of amyloid in the brain's blood vessels. It also did not cause any apparent inflammation or leaks in blood vessels in the animals' brains.
Finally, another set of experiments showed that the treated mice did not exhibit any memory decline when they were put into a radial arm maze, which evaluates working memory based on the animals' behavior.
The NYU researchers said they were encouraged that their synthetic peptide did not appear to cause inflammation or bleeding in the brains of the animals tested, and that the next step was transforming it into an agent that could be used clinically. "In order for a peptide like this to be used in humans it would have to be taken for many years, much like statin medications for cholesterol. Our ongoing research is now focusing on transforming the peptide used in the study into an agent that could be used clinically. It would have to be taken for a very long period of time without causing toxicity," Dr. Sadowski.
The study is published in the December 5, 2006, issue of the PNAS.
posted by Valery Yermalitsky at
6:20 AM
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