Abstract

Patients infected with human immunodeficiency virus (HIV-1) invariably experience a wide range of neurological complications associated with AIDS that are collectively referred to as HIV associated dementia (HAD). HIV associated dementia usually develops in advanced stages of HIV-1 disease. Clinically HAD involves varying degree of neurological and psychiatric symptoms like – cognitive impairment, motor disturbances, hallucinations, delirium and behavioural changes, often leading to progressive deterioration of cognitive and motor skills. The worldwide incidence of HAD is up to 40% of AIDS population. The advent of highly active anti-retroviral therapy (HAART) had a significant negative impact on HAD, nevertheless neurological complications had shown persistence. Variability in drug penetration, distribution, drug resistance, optimal dosage levels and toxicity, hinder the success of HAART in countering the neuronal cell death or damages to the brain. In the post HAART period a subtle form of HAD has evolved which is referred as minor cognitive motor disorder (MCMD). Hence the HIV-1 induced neurological complications continue to be a clinical problem amongst AIDS affected individuals. The aim of this review is to describe the cellular and molecular basis of neuropathogenesis of HAD, list the most common therapeutic regimens used in HAART, discuss briefly the advantages and limitations of HAART agents and describe how HAD has evolved in post HAART era. doi: 10.5214/ans.0972.7531.2007.140204

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