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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cognitive and functional outcomes are of primary interest in the design of efficacy trials in HIV-associated cognitive impairment. In a longitudinal cohort study, weak associations were found between measures of cognitive performance and commonly used measures of daily functioning (mostly self-report measures) in HIV-infected individuals. Modifications of current functional scales or new functional instruments are needed to assess the clinical relevance of cognitive changes in clinical trials of HIV-associated cognitive impairment.
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PMID:Clinical trials in HIV-associated cognitive impairment: cognitive and functional outcomes. 1117 16

The role of NFkappaB activation and its relationship to inflammatory mediators and apoptosis in the HIV-infected brain have remained uncertain. The cellular and regional distribution of NFkappaB, TNF-alpha, and apoptosis was examined in the frontal cortex (FC), deep white matter (DWM) and the basal ganglia (BG) of 17 patients with ADC. Nuclear staining for NFkappaB was localized predominantly to perivascular microglia/macrophages in the BG and DWM and correlated with ADC severity. Correlations were further found with HLA-DR, iNOS, TNF-alpha, and gp41 expression in these regions. The number of TUNEL-positive cells, particularly in the BG, correlated with ADC stage. Logistic regression analysis further showed a significant relationship between the likelihood of TUNEL staining in the BG and worsening cognitive impairment.
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PMID:NFkappaB activation, TNF-alpha expression, and apoptosis in the AIDS-Dementia-Complex. 1117 26

Approximately two thirds of patients with human immunodeficiency virus encephalitis (HIVE) show cognitive impairment and neurodegeneration, while one third are cognitively unimpaired and their neuronal populations are preserved. Thus, it is possible that these individuals might have the capacity to produce neurotrophic factors capable of protecting neurons against the deleterious effects of HIV. In this context, the main objective of this study was to determine whether fibroblast growth factor 1 (FGF1) is protective against HIV. For this purpose levels of FGF1 immunoreactivity were determined in the frontal cortex of 35 AIDS cases subdivided into 4 groups according to the presence or absence of HIVE and neurodegeneration. In cases without both HIVE and neurodegeneration, mild to moderate levels of FGFI immunoreactivity were observed in pyramidal neurons, while in cases with HIVE but without neurodegeneration, levels were significiantly elevated. In contrast, individuals with both HIVE and neurodegeneration showed low levels of neuronal FGF1 immunoreactivity. Furthermore, studies in primary human neuronal cultures treated with the HIV envelope protein-gp120 in the presence or absence of FGF1 showed that FGF1 was protective against gpl20 neurotoxicity in a dose-dependent manner. Taken together, these results support the notion that upregulation of certain neurotrophic factors, such as FGF1, might protect the central nervous system from the neurotoxic effects of HIV.
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PMID:Amelioration of neurotoxic effects of HIV envelope protein gp120 by fibroblast growth factor: a strategy for neuroprotection. 1124 13

Human immunodeficiency virus infection (HIV) at late stages of the disease is accompanied by neurological complications, including motor, behavioral and cognitive impairment. Using simian immunodeficiency virus (SIV)-infected rhesus monkeys, an animal model of HIV infection, we found that during the asymptomatic SIV infection dopamine (DA) deficits are early components of central nervous system (CNS) dysfunction. To investigate the role of the DA system in SIV infection and to restore the DA deficiency, we administered selegiline, an agent with DAergic and neuroprotective properties, to SIV-infected monkeys. Selegiline increased DA availability but induced CNS vacuolization, SIV encephalitic lesions, and enhanced CNS viral replication during early SIV infection. The pathological changes seem to be mediated by DA, as treatment with L-DOPA, the precursor of DA, had similar effects. We propose that any natural or induced DAergic dysregulation which results in increased DA availability may potentiate HIV-associated neurological disease (ND). Our findings raise new questions regarding the pathogenesis of HIV-ND and generate concerns about the safety of dopaminergic drugs in the clinical management of HIV-infected patients.
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PMID:Enhancement of central nervous system pathology in early simian immunodeficiency virus infection by dopaminergic drugs. 1127 77

It has been suggested that up to 15% of patients with AIDS may develop HIV-associated dementia. The syndrome may be either abrupt or insidious and is characterized by poor prognosis. Increasing cognitive impairment will necessitate the patient receiving a substantial amount of care and support in the community in addition to medical treatment and periods of hospitalization. The impact of caregiver burden is reasonably well documented in Alzheimer's disease, but there is a dearth of literature relating to caregiving and HIV-associated dementia. The current investigation is an observational study based on a small group of individuals which evaluates the experiences of these particular individuals as they care for their partner, friend, or son with HIV-associated dementia. The caregivers experience the stresses described in the non-HIV dementia literature; however, the nature of HIV disease means that there are issues involved in caring for this patient group that distinguish it from other types of dementia care; these include difficulties relating to specific HIV medical problems and problems with service shortfalls. The caregiver is more likely to be a parent or partner than a child of the patient due to the early age onset seen in this disease compared with Alzheimer's disease. Caregivers express their need for information about dealing with the everyday physical, behavioral, and emotional challenges and about services and benefits available. The interviewees expressed concerns over a perceived lack of communication and information from professionals involved in the patient's care and in the provision of services. The study offers an insight into the relevant issues affecting such caregivers and suggests areas of unmet needs that might be addressed in future service provisions.
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PMID:The burden of care: the impact of HIV-associated dementia on caregivers. 1136 87

Various vitamins and minerals play roles in HIV infection. There is evidence that a number of HIV+ patients suffer from deficiencies in vitamins B12, B6, A, and D; folate, zinc and selenium; and carotenoids such as beta-carotene, betacryptoxanthin, and lutein. Vitamin B12 deficiency can result in peripheral neuropathy, encephalopathy, cognitive dysfunction and anemia. Lowered levels of vitamins B6 and A can lead to impaired immune function and, in the latter, an increased rate of perinatal transmission. Low levels of vitamin D have been linked to weight loss and wasting. Folate deficiencies are related to anemia, and low levels of zinc and/or selenium have been linked to impaired immune function. Information on the carotenoids, which have been found to be associated with cellular immune function, is mostly derived from recent research. Studies have shown that the levels of carotenoids are decreased in HIV+ people even in the early stages of infection, but the greatest deficiencies appeared in patients with the most advanced disease. Other clinical trials seem to indicate that administration of beta-carotene improves immune function, causing an increase in CD4 counts over baseline levels. Clinical trials conducted in response to all of these deficiencies have found multivitamin supplementation to be beneficial. Therefore, it is recommended that all HIV-infected patients receive a multivitamin supplement to assist in reversing the damage caused by these vitamin and mineral deficiencies.
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PMID:Update on vitamins, minerals, and the carotenoids. 1136 98

A nationwide, eleven-site study has begun that uses injectable peptide T for HIV-associated cognitive impairment. The twelve-week, placebo-controlled study will measure peptide T's ability to help neurocognitive impairment by reducing brain levels of TNF-alpha, an immune system stimulant present in high levels during HIV infection.
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PMID:Peptide T for cognitive impairment. 1136 7

In a study conducted by the National Institutes of Health (NIH), open-label peptide T, a synthetic compound of eight amino acids, was found to be ineffective for the treatment of cognitive impairment in HIV-positive participants. Half of the 215 patients received 6 mg of peptide T intranasally for 6 months, the other half were given a placebo. All were placed on the drug for the following 6 months. Researchers measured overall neurological functions and seven cognitive functions, including memory and attention.
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PMID:Peptide T not effective for cognitive impairment. 1136 21

HIV-related cognitive impairment symptoms can include altered thoughts, emotions, and behaviors. Some aspects of cognitive impairment are treatable if addressed quickly, others are untreatable and progress rapidly. The fourfold response to cognitive impairment requires accurate diagnosis, treatment and education coordination, aggressive treatment of accute symptoms, and management through psychotherapy and psychopharmacology of untreatable symptoms. Mild impairment often occurs with minor motor impairment. Individuals with mild impairment have some slowness in thinking, memory, and problem-solving abilities, but usually live independently and continue to interact meaningfully with others. Psychotherapists should encourage individuals with mild HIV-related cognitive impairment to capitalize on strengths and compensate for limitations. Patients with moderate to severe cognitive impairment may have complete memory loss and impaired manipulation and information retrieval. The key intervention principle is to provide support.
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PMID:Treatment of cognitive impairment. 1136 52

The complexity of diagnosing cognitive impairment may be overwhelming. The diagnostic tools necessary to differentiate the causes of cognitive impairment are delineated. Most HIV-related cognitive impairment is caused by infection of the brain. Four HIV-related opportunistic conditions commonly cause cognitive impairment: toxoplasmosis, cryptococcal meningitis, progressive multifocal leukoencephalopathy, and lymphoma. Other causes are organic affective disorders, mood disturbances that result from specific biological causes. Some cognitive impairments are transient. Five procedures used to diagnose cognitive impairments are: mental status examination, neuropsychiatric interview, neurologic examination, laboratory and radiologic testing, and neuropsychological testing. These procedures may be conducted by a psychotherapist or a primary health care provider. Psychiatrists, neurologists, and neuropsychologists can be useful resources in negotiating the diagnostic process.
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PMID:Diagnosis of cognitive impairment. 1136 54


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