Positive and sustained effects of highly active antiretroviral therapy on HIV-1-associated neurocognitive impairment

Tozzi,; Balestra, Pietro; Galgani, Simonetta; Narciso, Pasquale; Ferri, Francesca; Sebastiani, Giovanni V.; D'Amato, C.; Affricano, Cesare; Pigorini, F; Fm, Pau; A, De Felici; Benedetto, A.

doi:10.1097/00002030-199910010-00011

Cited by 177 publications

(87 citation statements)

References 15 publications

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“…8 Subsequently, several observational studies independently reported significant NP improvements in patients receiving protease inhibitor (PI)-based HAART (Table 1). 27,28 Additional studies confirmed the finding in different populations including women 29,30 and patients in sub-Saharan Africa (Table 1). 31 Moreover, it was shown that the cognitive domains enhanced with HAART were psychomotor speed, verbal anterograde memory, and executive functions, thus supporting the idea that HAART could revert cognitive dysfunction by improving subcortical cognitive functions.…”

Section: Haart Improves Neurocognitive Functionsupporting

confidence: 76%

“…51 Most cohort studies also indicate that use of HAART is associated with improved cognition. 3,6,[26][27][28][29][30][31][32][33][34][35]37,38,[40][41][42]45,46,48,49,55,56 Interestingly, almost all randomized studies 8,24,25,36,50,51 and carefully designed prospective cohorts on advanced and/or cognitively impaired patients 30 in cognition with HAART use. Improvements were more pronounced in severely cognitively impaired subjects 48 and occur within a few weeks of ARV therapy initiation or change.…”

Section: Discussionmentioning

confidence: 99%

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Cognitive function in treated HIV patients

Tozzi¹

2010

NBHIV

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Although highly active antiretroviral therapy (HAART) has reduced the incidence of HIV-associated dementia, the overall prevalence of HIV-associated neurocognitive disorders (HAND) has increased. Since treatment and prevention of HAND are becoming an increasing concern, management strategies for cognitive impairment in patients living with HIV are expected to play an important role in the near future. This review summarizes the existing literature on studies investigating cognitive functions in patients receiving antiretroviral (ARV) treatment.Most studies indicate that HAART use results in improvement of neurocognitive functions, yet milder forms of HAND are not only prevalent, but also incident in patients with persistently undetectable plasma HIV RNA. We performed a systematic review on all studies performed in patients receiving ARV treatment that included neurocognitive evaluations as study end points. Thirty-six studies were examined. Study methodology varied from cross-sectional to doubleblind, randomized, controlled designs. Aside from historic zidovudine monotherapy trials, in most studies, ARV schemes varied considerably, and in some cases, ARV regimens were not reported in detail. Only a few articles included virological studies on cerebrospinal fluid. Study duration was ,2 years in most cases. Differences in study design and presence of study limitations may account for difficulties in understanding the impact of HAART on cognition and in evaluating the effect of an individual agent or ARV regimen on cognitive functioning. The aim of the present article is to provide HIV clinicians with a comprehensive review of recent achievements and future prospects for ARV treatment and prevention of cognitive dysfunctions in HIV-infected patients.

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Section: Haart Improves Neurocognitive Functionsupporting

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Cognitive function in treated HIV patients

Tozzi¹

2010

NBHIV

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“…It is widely believed HAD cognitive impairments are associated with the number of immune competent and HIV-1-infected MP (Glass et al 1995), diminished synaptic and dendritic density Everall et al 1999), and selective neuronal loss (Masliah et al 1992;Fox et al 1997). However, not all HAD patients exhibit profound neuronal loss (Seilhean et al 1993) and improvements in cognitive function have been observed after HAART (Ferrando et al 1998;Gendelman et al 1998;Tozzi et al 1999;Robertson et al 2004). This suggests that cognitive decline may result as much from neuronal dysfunction as from neuronal loss, an idea supported by experimental results showing alterations in cell layer volume and dendritic morphology ) correlate with HAD (Gray et al 2001).…”

Section: Introductionmentioning

confidence: 99%

Voltage-gated Potassium Channels in Human Immunodeficiency Virus Type-1 (HIV-1)-associated Neurocognitive Disorders

Keblesh

Xiong

2008

J Neuroimmune Pharmacol

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Human immunodeficiency virus type-1 (HIV-1)-associated dementia (HAD), a severe form of HIV-associated neurocognitive disorders (HAND), describes the cognitive impairments and behavioral disturbances which afflict many HIV-infected individuals. Although the precise mechanism leading to HAD is incompletely understood, it is commonly accepted its progression involves a critical mass of infected and activated mononuclear phagocytes (brain perivascular macrophages and microglia) releasing immune and viral products in the brain. These cellular and viral products induce neuronal dysfunction and injury via various signaling pathways. Emerging evidence indicates voltage-gated potassium (K v ) channels, key regulators of cell excitability and animal behavior (learning and memory), are involved in the pathogenesis of HAD/HAND. Here we survey the literature and find that HAD-related alterations in cellular and viral products can increase neuronal K v channel activity, leading to neuronal dysfunction and cognitive deficits. Thus, neuronal K v channels may be a new target in the effort to develop therapies for HAD and perhaps other inflammatory neurodegenerative disorders.

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“…Antiretroviral therapy has dramatically reduced the incidence and severity of opportunistic infections associated with HIV and improved neurocognitive function [1,2], but it remains unclear how effectively antiretroviral therapy protects the CNS against HIV-related disease. Many investigators have used event-related brain potentials (ERPs) to assess CNS function in HIV patients; however, most of have focused on phasic components such as the P300.…”

Section: Introductionmentioning

confidence: 99%

Abnormal contingent negative variation in HIV patients receiving antiretroviral therapy

Chao¹,

Cardenas²,

Meyerhoff³

et al. 2003

NeuroReport

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The contingent negative variation, an event-related potential related to neural activity in the frontal lobe and basal ganglia, neuropsychological tests and structural MRI were used to examine CNS function and structure in HIV-positive patients receiving antiretroviral therapy. Relative to controls, HIV patients had smaller thalamic volume and reduced late contingent negative variation amplitude that correlated with caudal atrophy. Behaviorally, viremic patients were more impaired than virally suppressed patients and controls on neuropsychological measures of psychomotor speed, selective attention and mental flexibility. These results suggest that antiretroviral therapy may not be effective in protecting cortical and subcortical structures against HIV-related neuropathology, regardless of immune function. However, the benefits of antiretroviral therapy on immune function appear to facilitate neurocognitive performance.

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Positive and sustained effects of highly active antiretroviral therapy on HIV-1-associated neurocognitive impairment

Abstract: HAART produces a positive and sustained effect on neurocognitive impairment in HIV-infected patients. A reduction of plasma viral load was associated with the regression of neuropsychological test abnormalities.

Cited by 177 publications

References 15 publications

Cognitive function in treated HIV patients

Cognitive function in treated HIV patients

Voltage-gated Potassium Channels in Human Immunodeficiency Virus Type-1 (HIV-1)-associated Neurocognitive Disorders

Abnormal contingent negative variation in HIV patients receiving antiretroviral therapy

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