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December 31, 2001
Both HIV and Alzheimer’s disease can damage the brain, but most people think the similarity between the two ends there. Recent research from San Francisco Veterans Affairs Medical Center (SFVAMC) suggests a closer connection. They have found the brain damage from both diseases appears to involve inflammation, suggesting that anti-inflammatory drugs could help relieve symptoms.
The latest findings to support this link show that AIDS dementia, like Alzheimer’s, may now be a chronic condition. The study, published in the latest issue of the journal AIDS, shows that immune cell markers of AIDS dementia remain even after a patient is treated with anti-retroviral drug cocktails. These same markers are elevated in patients with Alzheimer’s disease.
“The brain wages an immune response against HIV infection. We believe that the brain is damaged by inflammatory toxins that are released as part of the brain’s immune response. The amyloid plaques of Alzheimer’s are also believed to cause a toxic inflammatory response,” said lead author Lynn Pulliam, PhD, chief of microbiology at SFVAMC and University of California, San Francisco, professor of laboratory medicine and medicine.
According to cell culture studies published earlier this year in the journal Brain Research, certain anti-inflammatory drugs may be able to reduce the damage from these toxins. The brains of AIDS dementia patients have increased numbers of immune cells called monocyte/macrophages, which secrete chemicals that are toxic to cultured brain cells. The study found that treatment with an experimental anti-inflammatory drug prevented this toxicity.
The drug, called CPI-1189, has been tested on patients with AIDS dementia in preliminary Phase II clinical trials, and it appears to improve patients’ performance on tests of psychomotor and cognitive function.
“It would be very exciting if anti-inflammatory drugs turn out to be an effective additional treatment for AIDS dementia, or for Alzheimer’s disease, because it would be a relatively simple approach that we already understand to some degree,” Pulliam said.
Recent research from other investigators has suggested that non-steroidal anti-inflammatory drugs, such as ibuprofin, may help to delay the onset of Alzheimer’s disease, further supporting the importance of inflammation in both AIDS dementia and Alzheimer’s.
The new study from Pulliam’s group focuses on a subset of monocyte/macrophages that are more numerous in both AIDS dementia and in Alzheimer’s disease. Monocyte/macrophages that display a surface molecule called CD69 are much more prolific in the blood of AIDS dementia patients and patients with Alzheimer’s disease than in healthy people.
The research showed after AIDS dementia patients were treated with a complete anti-AIDS drug regimen, their levels of CD69 cells were somewhat lower but still higher than non-demented AIDS patients and similar to those of patients with Alzheimer’s disease. This neurotoxicity appears to alter levels of important structural and functional proteins in the brain.
“It appears that HIV-associated dementia has evolved into a more protracted disorder. Although treatment with anti-retroviral drugs appears to cause macrophages monocyte/macrophages to secrete lower levels of toxins, a more subtle neurotoxicity continues to disable neurons,” Pulliam said.
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