David B Clifford1. 1. Washington University in St Louis, 660 South Euclid Avenue, St Louis, Missouri, USA.
Abstract
PURPOSE OF REVIEW: HIV-associated neurocognitive disease is the most active topic for neuroAIDS investigations at present. Although impairment is mild in patients successfully treated with modern antiviral regimens, it remains an ongoing problem for HIV patients. It is important to update the emerging research concerning HIV-associated neurocognitive disease. RECENT FINDINGS: The virus enters the brain during acute infection, with evidence for abnormal functioning that may occur early and often persists. Direct relationships with ongoing viral infection continue to be monitored, but chronic inflammation often associated with monocytes and macrophages appears to be the most likely driver of cognitive dysfunction. Appreciation for cerebrovascular disease as a significant comorbidity that is associated with cognitive deficits is increasing. Neuroimaging is actively being developed to address detection and measurement of changes in the brain. Optimal combined antiretroviral treatment therapy has vastly improved neurologic outcomes, but so far has not been demonstrated to reverse the remaining mild impairment. Inflammatory and vascular mechanisms of cerebral dysfunction may need to be addressed to achieve better outcomes. SUMMARY: Ongoing research is required to improve neurological outcomes for persons living with HIV. It is likely that interventions beyond antiviral approaches will be required to control or reverse HIV-associated neurocognitive disease.
PURPOSE OF REVIEW: HIV-associated neurocognitive disease is the most active topic for neuroAIDS investigations at present. Although impairment is mild in patients successfully treated with modern antiviral regimens, it remains an ongoing problem for HIVpatients. It is important to update the emerging research concerning HIV-associated neurocognitive disease. RECENT FINDINGS: The virus enters the brain during acute infection, with evidence for abnormal functioning that may occur early and often persists. Direct relationships with ongoing viral infection continue to be monitored, but chronic inflammation often associated with monocytes and macrophages appears to be the most likely driver of cognitive dysfunction. Appreciation for cerebrovascular disease as a significant comorbidity that is associated with cognitive deficits is increasing. Neuroimaging is actively being developed to address detection and measurement of changes in the brain. Optimal combined antiretroviral treatment therapy has vastly improved neurologic outcomes, but so far has not been demonstrated to reverse the remaining mild impairment. Inflammatory and vascular mechanisms of cerebral dysfunction may need to be addressed to achieve better outcomes. SUMMARY: Ongoing research is required to improve neurological outcomes for persons living with HIV. It is likely that interventions beyond antiviral approaches will be required to control or reverse HIV-associated neurocognitive disease.
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