Jan J Krut1, Richard W Price2, Henrik Zetterberg3,4, Dietmar Fuchs5, Lars Hagberg1, Aylin Yilmaz1, Paola Cinque6, Staffan Nilsson7, Magnus Gisslén1. 1. a Department of Infectious Diseases , Institute of Biomedicine, University of Gothenburg , Gothenburg , Sweden. 2. b Department of Neurology , University of California San Francisco , San Francisco , CA , USA. 3. c Department of Psychiatry and Neurochemistry , Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg , Gothenburg , Sweden. 4. d UCL Institute of Neurology , London , UK. 5. e Division of Biological Chemistry , Biocenter, Innsbruck Medical University , Innsbruck , Austria. 6. f Clinic of Infectious Diseases , San Raffaele Hospital , Milan , Italy. 7. g Department of Mathematical Sciences , Chalmers University of Technology , Gothenburg , Sweden.
Abstract
BACKGROUND: The prevalence of neurocognitive deficits are reported to be high in HIV-1 positive patients, even with suppressive antiretroviral treatment, and it has been suggested that HIV can cause accelerated aging of the brain. In this study we measured phosphorylated tau (p-tau) in cerebrospinal fluid (CSF) as a potential marker for premature central nervous system (CNS) aging. P-tau increases with normal aging but is not affected by HIV-associated neurocognitive disorders. METHODS: With a cross-sectional retrospective design, p-tau, total tau (t-tau), neopterin and HIV-RNA were measured in CSF together with plasma HIV-RNA and blood CD4+ T-cells of 225 HIV-infected patients <50 y of age, subdivided into 3 groups: untreated neuroasymptomatic (NA) (n = 145), on suppressive antiretroviral treatment (cART) (n = 49), and HIV-associated dementia (HAD) (n = 31). HIV-negative healthy subjects served as controls (n = 79). RESULTS: P-tau was not significantly higher in any HIV-infected group compared to HIV-negative controls. Significant increases in t-tau were found as expected in patients with HAD compared to NA, cART, and control groups (p < 0.001 ). CONCLUSIONS: P-tau was not higher in HIV-infected patients compared to uninfected controls, thus failing to support a role for premature or accelerated brain aging in HIV infection.
BACKGROUND: The prevalence of neurocognitive deficits are reported to be high in HIV-1 positive patients, even with suppressive antiretroviral treatment, and it has been suggested that HIV can cause accelerated aging of the brain. In this study we measured phosphorylated tau (p-tau) in cerebrospinal fluid (CSF) as a potential marker for premature central nervous system (CNS) aging. P-tau increases with normal aging but is not affected by HIV-associated neurocognitive disorders. METHODS: With a cross-sectional retrospective design, p-tau, total tau (t-tau), neopterin and HIV-RNA were measured in CSF together with plasma HIV-RNA and blood CD4+ T-cells of 225 HIV-infectedpatients <50 y of age, subdivided into 3 groups: untreated neuroasymptomatic (NA) (n = 145), on suppressive antiretroviral treatment (cART) (n = 49), and HIV-associated dementia (HAD) (n = 31). HIV-negative healthy subjects served as controls (n = 79). RESULTS: P-tau was not significantly higher in any HIV-infected group compared to HIV-negative controls. Significant increases in t-tau were found as expected in patients with HAD compared to NA, cART, and control groups (p < 0.001 ). CONCLUSIONS: P-tau was not higher in HIV-infectedpatients compared to uninfected controls, thus failing to support a role for premature or accelerated brain aging in HIV infection.
Entities:
Keywords:
HIV; HIV-1 associated cognitive motor complex; biomarker analysis; cerebrospinal fluid; tau protein
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