Markers of macrophage activation and axonal injury are associated with prospective memory in HIV-1 disease
Title | Markers of macrophage activation and axonal injury are associated with prospective memory in HIV-1 disease |
Publication Type | Journal Article |
Year of Publication | 2006 |
Authors | Woods, SPaul, Morgan, EE, Marquie-Beck, J, Carey, C, Grant, I, Letendre, S |
Journal | Cognitive and Behavioral Neurology: Official Journal of the Society for Behavioral and Cognitive Neurology |
Volume | 19 |
Pagination | 217-21 |
Date Published | 2006 |
Keywords | Adult, Axons, Biological Markers, Chemokine CCL2, Female, Fibroblast Growth Factor 1, HIV Infections, HIV-1, Humans, Immunoglobulin G, Internal, Macrophages, Male, Memory, Memory Disorders, Middle Aged, Receptors, RNA, Statis, Tumor Necrosis Factor, Viral |
Abstract | OBJECTIVE: To use clinical specimens to better understand the neuropathogenesis of prospective memory (ProM) functioning in persons with HIV-1 infection. BACKGROUND: Emergent evidence suggests that HIV-1 is associated with impaired ProM, but the underlying neuropathophysiology of this deficit is not known. METHODS: Thirty-five nondemented subjects with HIV-1 infection completed measures of both ProM (ie, memory for future intentions) and retrospective memory (RM; ie, memory for past episodes). A panel of biomarkers reflecting several possible neuropathogenic mechanisms of HIV was measured in plasma and cerebrospinal fluid, including HIV-1 RNA, total tau, monocyte chemoattractant protein-1 (MCP-1), soluble receptor for tumor necrosis factor type II, and fibroblast growth factor 1. RESULTS: After controlling for antiretroviral therapy and CD4 lymphocyte count, higher levels of MCP-1 in plasma, and soluble receptor for tumor necrosis factor type II and tau in cerebrospinal fluid were associated with ProM, but not RM. Markers of astrocytosis, growth factor depletion, and HIV-1 replication did not predict either ProM or RM. CONCLUSIONS: ProM impairment in HIV-1 may be dissociable from RM, perhaps reflecting specific neuropathogenic mechanisms of macrophage activation and axonal injury. |
URL | http://www.ncbi.nlm.nih.gov/pubmed/17159619 |