No support for premature central nervous system aging in HIV-1 when measured by cerebrospinal fluid phosphorylated tau (p-tau). Issue 5 (4th July 2017)

• Record Type: Journal Article
• Authors: Krut, Jan J.; Price, Richard W.; Zetterberg, Henrik; Fuchs, Dietmar; Hagberg, Lars; Yilmaz, Aylin; Cinque, Paola; Nilsson, Staffan; Gisslén, Magnus
• Is Part Of: Virulence. Volume 8:Issue 5(2017)
• Page Start: 599
• Page End: 604
• Publication Date: 2017-07-04
• Subjects: biomarker analysis -- cerebrospinal fluid -- HIV -- HIV-1 associated cognitive motor complex -- tau protein; Virulence (Microbiology) -- Periodicals; Bacterial diseases -- Periodicals; Molecular microbiology -- Periodicals; 579.05
• DOI: 10.1080/21505594.2016.1212155
• Languages: English
• ISSNs: 2150-5608

Abstract

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.