Neuropathological sequelae of Human Immunodeficiency Virus and apathy: A review of neuropsychological and neuroimaging studies. (August 2015)

• Record Type: Journal Article
• Authors: McIntosh, Roger C.; Rosselli, Monica; Uddin, Lucina Q.; Antoni, Michael
• Is Part Of: Neuroscience and biobehavioral reviews. Volume 55(2015:Aug.)
• Page Start: 147
• Page End: 164
• Publication Date: 2015-08
• Subjects: Human Immunodeficiency Virus -- Apathy -- Neurocognitive impairment -- MRI -- DTI -- Functional connectivity -- Neuropsychiatric dysfunction; Psychophysiology -- Periodicals; Human behavior -- Periodicals; Animal behavior -- Periodicals; Neurology -- Periodicals; Behavior -- Periodicals; Ethology -- Periodicals; Neurology -- Periodicals; Psychophysiologie -- Périodiques; Comportement humain -- Périodiques; Animaux -- Mœurs et comportement -- Périodiques; Neurologie -- Périodiques; Animal behavior; Human behavior; Neurology; Psychophysiology; Periodicals; Electronic journals; 573.8
• DOI: 10.1016/j.neubiorev.2015.04.008
• Languages: English
• ISSNs: 0149-7634

Abstract

Highlights: HIV induces neurotoxic effects on dopaminergic neurons and glia via viral proteins, e.g., Tat and gp120. Morphometric and functional imaging shows apathy severity in HIV reflects frontal-striatal pathology. HIV-associated neurocognitive impairments also suggest apathy also relates to disruption of this extended network. Abstract: Apathy remains a common neuropsychiatric disturbance in the Human Immunodeficiency Virus (HIV-1) despite advances in anti-retroviral treatment (ART). The goal of the current review is to recapitulate findings relating apathy to the deleterious biobehavioral effects of HIV-1 in the post-ART era. Available literatures demonstrate that the emergence of apathy with other neurocognitive and neuropsychiatric symptoms may be attributed to neurotoxic effects of viral proliferation, e.g., aggregative effect of Tat and gp120 on apoptosis, transport and other enzymatic reactions amongst dopaminergic neurons and neuroglia. An assortment of neuroimaging modalities converge on the severity of apathy symptoms associated with the propensity of the virus to replicate within frontal-striatal brain circuits that facilitate emotional processing. Burgeoning research into functional brain connectivity also supports the effects of microvascular and neuro-inflammatory injury linked to aging with HIV-1 on the presentation of neuropsychiatric symptoms. Summarizing these findings, we review domains of HIV-associated neurocognitive and neuropsychiatric impairment linked to apathy in HIV. Taken together, these lines of research suggest that loss of affective, cognitive and behavioral inertia is commensurate with the neuropathology of HIV-1.