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Even Mild Infections Hasten Decline With Alzheimer's
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Page: << Prev | 1 | 2 | 3 | Next >> "The effect of these illnesses on memory function is most marked in subjects who also have existing chronic inflammatory conditions," Holmes said. "Here, the rate of memory decline is 10-fold. We believe the signal is coming from these illnesses and being sent to the brain by TNF-a, a protein known to be associated with a range of inflammatory conditions," he said.
For those whose TNF-a levels were high at the start of the study, an infection increased their memory loss 10 times over those who had low TNF-a levels, the study authors found.
Greater care is needed to prevent these conditions occurring in people with Alzheimer's disease, Holmes said.
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"Thus the use of influenza vaccinations should be encouraged, and early treatment of infections may reduce the deleterious effect of these infections," he said.
"Finally, the development of drugs or lifestyle changes, such as moderate exercise that has been shown to reduce TNF-a in patients with Alzheimer's disease, are worth examining for their beneficial effects on slowing down the disease process," Holmes said.
Greg M. Cole, associate director of the Alzheimer's Disease Research Center at UCLA David Geffen School of Medicine, said this is a very interesting study associating episodes of infectious disease with increases in a pro-inflammatory molecule in blood and rates of cognitive decline in people who already have Alzheimer's disease.
"Like all association studies, it does not prove causal relationships," Cole said. "However, it makes some sense because the molecule they measure in blood, TNF-a, is known to traffic from the blood to trigger increased brain inflammation in animal models, and has been a candidate target for disease intervention," he said.
However, common anti-inflammatory medications, such as Celebrex or Aleve, have generally failed to slow disease progression in clinical trials, Cole said.
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Copyright © 2009 ScoutNews, LLC. All rights reserved.
Last updated 9/8/2009
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SOURCES: Clive Holmes, MRCPsych, Ph.D., Clinical Neurosciences Research Division, University of Southampton, U.K.; Greg M. Cole, Ph.D., neuroscientist, Greater Los Angeles VA Healthcare System, and associate director, Alzheimer's Disease Research Center, UCLA David Geffen School of Medicine; Maria Carrillo, Ph.D., director, medical and scientific relations, Alzheimer's Association; Sept. 8, 2009, Neurology
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