Aspectos moleculares de la demencia asociada con el SIDA

A variety of neuropsychiatric disorders have been described in 20 to 30 % of the patients suffering of acquired immunodeficiency syndrome (AIDS). Due to the fact that neurons are not directly infected with the human immunodeficiency virus (HIV), the pathophysiological manifestations of the AIDS-related dementia complex (ADC) could be mediated through indirect mechanisms. The envelope glycoprotein 120 (gp120) derived from HIV seems to play an important role in the development of ADC. A number of experiments have shown that a nanomolar concentration of gp 120 derived from HIV produces neuronal dead in vivo, and picomolar concentration kills neurons in vitro. Recent data suggest that in order to induce neuronal damage the citokines and CD4+ receptor play an important role in the activation of intracellular events that lead to an increase of intracellular Ca⁺⁺ through the NMDA receptors, consequently triggering intracellular events and apoptosis. Understanding the mechanism causing neuronal damage at molecular and behavioral level, very likely will provide clues for treatment and prevention of this clinical entity. In this review we include the development of animal models which are useful to study the mechanisms of AIDS related dementia complex.