Abstract
ObjectiveMild neurocognitive disorders (MND) affect a subset of HIV+ patients under effective combination antiretroviral therapy (cART). In this study, we used an innovative multi-contrast magnetic resonance imaging (MRI) approach at high-field to assess the presence of micro-structural brain alterations in MND+ patients.MethodsWe enrolled 17 MND+ and 19 MND− patients with undetectable HIV-1 RNA and 19 healthy controls (HC). MRI acquisitions at 3T included: MP2RAGE for T1 relaxation times, Magnetization Transfer (MT), T2* and Susceptibility Weighted Imaging (SWI) to probe micro-structural integrity and iron deposition in the brain. Statistical analysis used permutation-based tests and correction for family-wise error rate. Multiple regression analysis was performed between MRI data and (i) neuropsychological results (ii) HIV infection characteristics. A linear discriminant analysis (LDA) based on MRI data was performed between MND+ and MND− patients and cross-validated with a leave-one-out test.ResultsOur data revealed loss of structural integrity and micro-oedema in MND+ compared to HC in the global white and cortical gray matter, as well as in the thalamus and basal ganglia. Multiple regression analysis showed a significant influence of sub-cortical nuclei alterations on the executive index of MND+ patients (p = 0.04 he and R2 = 95.2). The LDA distinguished MND+ and MND− patients with a classification quality of 73% after cross-validation.ConclusionOur study shows micro-structural brain tissue alterations in MND+ patients under effective therapy and suggests that multi-contrast MRI at high field is a powerful approach to discriminate between HIV+ patients on cART with and without mild neurocognitive deficits.
Highlights
It has been suggested that HIV encephalitis is the neuropathological substrate of cognitive disorders [1]
Mild neurocognitive disorders (MND)+ and MND2 groups did not differ in age, gender, educational level and HIV-characteristics (Table 2)
Univariate analysis showed (i) lower Magnetization Transfer Ratio (MTR) in WM, cGM, thalamus and caudate as well as (ii) lower T1 in all regions but the thalamus when MND+ patients where compared to healthy controls (HC)
Summary
It has been suggested that HIV encephalitis is the neuropathological substrate of cognitive disorders [1]. HIV does not directly infect neurons or oligodendrocytes, this virus can trigger an inflammatory response with release of cytokines, chemokines, and neurotoxic HIV viral proteins (e.g. gp120). Combination antiretroviral therapy (cART) may not be sufficient to prevent neuro-inflammatory damages triggered by HIV since some anti-retroviral drugs have a poor rate of penetration-effectiveness into the central nervous system (CNS) [6]. Some cART compounds with good penetration might be neurotoxic and provoke cognitive disorders in patients with long-standing treatment [7,8]. We used a multi-contrast approach at 3 T in a population of HIV patients well treated with cART (undetectable viral load) with and without cognitive impairments (MND+ and MND2) as well as a population of healthy sero-negative controls (HC)
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