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Abstract

HIV-associated dementia (HAD) and milder forms of impairment, now termed HIV-associated neurocognitive disorders (HAND), still occur despite the introduction of highly active antiretroviral therapy (HAART).1 There are numerous reasons: delayed commencement of, or resistance to HAART, inadequate response to HAART because of poor CNS penetration, as a manifestation of HAART-induced immune restoration, and because of inactive or burnt out disease. As Schifitto et al.2 point out, there is some evidence of continuing oxidative stress in the CNS despite optimal treatment with HAART. This has formed the rationale for adjunctive therapy with a neuroprotectant aimed at reducing such oxidative stress. The article by Schifitto et al. in this issue2 reports their findings. The study was a three-arm, placebo-controlled examination of the efficacy of transdermal selegiline in two doses (3 mg/24 hours and 6 mg/24 hours) on HIV-related cognitive deficits. Selegiline was chosen as it can decrease oxygen-free radicals, increase the formation of the antioxidant enzymes superoxide dismutase and catalase, and enhance the synthesis of certain neurotrophic factors. Moreover, two previous placebo-controlled pilot studies of oral and transdermal selegiline in subjects with HIV-associated cognitive impairment had suggested improvement in several tests of psychomotor speed. In the current study …