The aging of human-immunodeficiency-virus-associated neurocognitive disorders.

This special issue proposes a new era for studies of the humanimmunodeficiency-virus-type-one (HIV-1) -associated neurological disorders serving to highlight cognitive abnormalities in infected aging patients. It has been 15 years since the “Third Workshop on NeuroAIDS” was held (Black and Sager 1994). At that time, NeuroAIDS (or the AIDS dementia complex) was the principal manifestation of cognitive, behavioral, and motor abnormalities in patients with the acquired immunodeficiency syndrome (AIDS). This has all but changed. Indeed, after introduction of highly active antiretroviral therapy (HAART) in 1996 and1997, the prevalence of severe manifestations of NeuroAIDS was significantly reduced, and the HIV patients show reduced disease morbidities and mortality. According to the Centers for Disease Control, the number of people 50 years and older infected with HIV has increased from 77% from 2001 to 2005. As HIV disease becomes a treatable medical disorder, morbidities in the HAART era abound including those linked to antiretroviral toxicities and viral infection per se as well as common disorders that all aging patients face, such as chronic obstructive pulmonary disease, diabetes, atherosclerosis-linked heart, vascular and kidney failure, bleeding ulcers, depression, cancers, and osteoporosis. Recent studies on aged HIV patient brain suggest a new type of neurological disorders distinct from HIV-1-associated dementia (HAD) and now termed HIV-associated neurocognitive disorders (HAND). HAND in aged population is linked, in part, to early signs of beta-amyloidosis or microtubule-associated tau aggregation commonly seen in Alzheimer’s disease (AD) or tauopathy brain. However, whereas extracellular amyloid plaques (senile plaques) are the major amyloid pathology in AD, HAND brains show intraneuronal amyloid accumulation or perivascular diffuse amyloid deposition, indicating distinct mechanisms and brain disease development. Considering the increase in the aged HIV population, this issue of the Journal of Neuroimmune Pharmacology will specifically focus for the first time on age-associated neurodegeneration in HIV patients. Special emphasis was made on beta-amyloidosis contributed by an outstanding line of seven investigators representing the cutting edge of HAND research activities. Peer-reviewed original research and review articles provide clear direction for forthcoming HAND research directives. The issue is lead by a comprehensive review of neurodegeneration and aging in the HAART era (Brew et al. 2009). This review discusses the history of NeuroAIDS, HAART, and persistent neurodegeneration in HAARTtreated patients. The implication of neurodegeneration in post-HAART patients is provocative and highlighted in its association with HIV, aging, and inflammation. Potential mechanisms common to specific diseases, such as AD and Parkinson’s disease, and therapeutic inventions are proposed. HAND pathogenesis, in the context of selective vulnerability of specific neuronal populations, epidemiology, and risk factors, is reviewed by Jayadev and Garden (2009). This article discusses a variety of host and viral factors that are associated with increased risk of developing HAND, and some of which are associated with the development of AD. Here, they propose a different view of how viral J Neuroimmune Pharmacol (2009) 4:161–162 DOI 10.1007/s11481-009-9155-5