ABSTRACT
HIV-1-associated dementia (HAD) involves nearly 15 to 20% of patients infected with AIDS (1). It is known as a metabolic encephalopathy induced by viral infection of brain mononuclear phagocytes (MPs) (perivascular and parenchymal brain macrophages/microglia) and continues through paracrine-amplified, inflammatory, and neurotoxic reactions. HAD has been defined clinically by the impediment of concentration, distorted cognition, slowness of movement, and behavioral changes (2). In the central nervous system, macrophages and resident microglia constitute a cellular reservoir of HIV-1, presenting a safe haven for virus, so that we will likely observe virus and host-coded producing neurotoxins in HAD (3). The neurotoxic activity has been characterized in many experiments via N-methyl aspartate (NMDA) receptors (4,5). Many researchers have reported that the probable causes are as follows: the virion protein toxin candidates NTox (6), platelet activating factor (7), tumor necrosis factor alpha (TNF-α) (8), quinolinate (9), Tat (10), gp120 (11), and gp41 (12). Furthermore, the strength of these toxins is in HIV-infected macrophage secretions, cerebrospinal fluid, or most likely within the brain tissues of subjects infected with HIV-1.
