RESUMO
BACKGROUND: Cardiovascular disease (CVD) and premature aging have been hypothesized as new risk factors for HIV associated neurocognitive disorders (HAND) in adults with virally-suppressed HIV infection. Moreover, their significance and relation to more classical HAND biomarkers remain unclear. METHODS: 92 HIV- infected (HIV+) adults stable on combined antiretroviral therapy (cART) and 30 age-comparable HIV-negative (HIV-) subjects underwent (1)H Magnetic Resonance Spectroscopy (MRS) of the frontal white matter (targeting HIV, normal aging or CVD-related neurochemical injury), caudate nucleus (targeting HIV neurochemical injury), and posterior cingulate cortex (targeting normal/pathological aging, CVD-related neurochemical changes). All also underwent standard neuropsychological (NP) testing. CVD risk scores were calculated. HIV disease biomarkers were collected and cerebrospinal fluid (CSF) neuroinflammation biomarkers were obtained in 38 HIV+ individuals. RESULTS: Relative to HIV- individuals, HIV+ individuals presented mild MRS alterations: in the frontal white matter: lower N-Acetyl-Aspartate (NAA) (p<.04) and higher myo-inositol (mIo) (p<.04); in the caudate: lower NAA (pâ=â.01); and in the posterior cingulate cortex: higher mIo (p<.008- also significant when Holm-Sidak corrected) and higher Choline/NAA (p<.04). Regression models showed that an HIV*age interaction was associated with lower frontal white matter NAA. CVD risk factors were associated with lower posterior cingulate cortex and caudate NAA in both groups. Past acute CVD events in the HIV+ group were associated with increased mIo in the posterior cingulate cortex. HIV duration was associated with lower caudate NAA; greater CNS cART penetration was associated with lower mIo in the posterior cingulate cortex and the degree of immune recovery on cART was associated with higher NAA in the frontal white matter. CSF neopterin was associated with higher mIo in the posterior cingulate cortex and frontal white matter. CONCLUSIONS: In chronically HIV+ adults with long-term viral suppression, current CVD risk, past CVD and age are independent factors for neuronal injury and inflammation. This suggests a tripartite model of HIV, CVD and age likely driven by chronic inflammation.
Assuntos
Envelhecimento/patologia , Lesões Encefálicas/diagnóstico , Doenças Cardiovasculares/complicações , Infecções por HIV/diagnóstico , HIV/fisiologia , Espectroscopia de Ressonância Magnética , Prótons , Adulto , Afeto , Terapia Antirretroviral de Alta Atividade , Biomarcadores/líquido cefalorraquidiano , Encéfalo/patologia , Lesões Encefálicas/líquido cefalorraquidiano , Lesões Encefálicas/complicações , Lesões Encefálicas/fisiopatologia , Cognição , Demografia , Feminino , Infecções por HIV/líquido cefalorraquidiano , Infecções por HIV/complicações , Infecções por HIV/tratamento farmacológico , Humanos , Masculino , Pessoa de Meia-Idade , Testes Neuropsicológicos , Fatores de RiscoRESUMO
OBJECTIVE: To examine facial emotional processing in HIV+ individuals and its relation to neurocognitive performance, neuropsychiatric symptomatology and immune status. METHOD: Participants included 85 HIV+ individuals (83 males, 2 females) and 25 age-comparable HIV- individuals (22 males, 3 females). Participants underwent The University of Pennsylvania computerized neuropsychological facial emotion test battery, standardized neuropsychological testing, neurobehavioral questionnaires, a semistructured psychiatric interview, and an assessment of independence in activities of daily living. RESULTS: Relative to HIV- controls, HIV+ individuals showed a mild difference for recognition of sadness (p = .02, d = 0.43), discrimination of happiness (p = .02, d = 0.52), and speed of recognition for fear (p = .04, d = 0.37). HIV+ individuals with HIV-associated neurocognitive disorder (HAND; 20%) had abnormal emotional facial recognition (p = .04; d = .59), and slower recognition of negative facial expressions (p < .01; d = .63-.83), as well as poorer discrimination of happy facial expressions (p < .003, d = .83). Apathy, depression, reduced independence in activities of daily living, and HIV biomarkers were not associated with reduced facial emotion recognition in the HIV+ group. CONCLUSIONS: Clinically stable HIV+ individuals show a mild level of emotional processing reduction that is dissociated from neuropsychiatric complaints. Individuals with HAND showed moderate to large emotional processing abnormalities, particularly for the timely recognition of negative expressions (fear, sadness, and anger). These findings warrant a more comprehensive and dynamic evaluation of emotional processing in HIV infection and an investigation of the integrity of the fronto-basal-amygdala circuits.