"Our study shows that there may be no overlap between biomarkers that can predict the onset of neurodegenerative disease in HIV-infected patients and markers that are associated with disease progression," Dr. Norman J. Haughey from Johns Hopkins University School of Medicine, Baltimore, Maryland told Reuters Health.

Dr. Haughey and colleagues note that traditional biomarkers such as HIV load in cerebrospinal fluid are less likely to be associated with HIV dementia nowadays, and others have yet to be identified.

The researchers sought to determine whether changes in sphingolipid, sterol, and oxidant balance in cerebrospinal fluid are associated with HIV dementia and can predict changes in the cognitive status. CSF samples were obtained from 48 patients, who were categorized for neuropsychological function on three visits.

Accumulations of tocopherol and triglyceride C52 predicted the onset or worsening of dementia, the researchers report.

Patients with inactive dementia had significant increases in sphingomyelin, compared with sphingomyelin concentrations in patients with active dementia or no dementia, they found.

In contrast, active dementia was associated with increases in ceramide, "suggesting that a conversion of sphingomyelin to ceramide is associated with progression of dementia."

The team writes: "We interpret these findings to indicate that early in the pathogenesis of HIV dementia, there is up-regulation of endogenous antioxidant defenses in brain. The failure of this attempted neuroprotective mechanism leads to the accumulation of sphingomyelin and moderate cognitive dysfunction. The breakdown of this enlarged pool of sphingomyelin to ceramide and the accumulation of highly reactive aldehydes are associated with declining cognitive function."

Dr. Haughey added, "We are currently verifying the use of sphingomyelins and ceramides to track disease progression and the effectiveness of therapeutics in ongoing clinical trials for HIV-dementia and Alzheimer's disease."

Neurology 2007;68:1481-1487.

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