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PubMed1997

Tumor necrosis factor-alpha, microglia and astrocytes in AIDS dementia complex.

The pathogenesis of HIV-associated cognitive changes is poorly understood. Cytokines such as tumor necrosis factor-alpha (TNF-alpha) have been postulated to contribute to the mechanism of the neurological complications of HIV infection. One of the effects of TNF-alpha is to induce astrocyte proliferation in vitro. The purpose of this study was to look for a correlation between the expression of TNF-alpha, astrogliosis and the degree of cognitive impairment in 12 prospectively assessed AIDS cases without focal brain lesion, 8 of whom were demented. They were compared with 6 control patients without neurological disease. Neuropathological examination showed myelin pallor in 5 of the 8 demented patients. TNF-alpha expression was detected by immunohistochemistry in the midfrontal cortex, subcortical and deep white matter, and basal ganglia. Not only perivascular macrophages but also some microglial and endothelial cells were labeled. Most TNF-alpha-positive cells were in close contact with glial fibrillary acidic protein-positive astrocytes. They were more numerous than gp41-positive cells. Their density increased with increasing cognitive impairment and in parallel to the astrogliosis in the frontal cortex, basal ganglia and deep white matter. These findings further support the hypotheses that lesions of the deep white matter, driven by TNF-alpha, are associated with cognitive alteration, and that indirect effects of HIV infection in the brain participate in the development of HIV-associated dementia through a diffuse immune activation, mediated by cytokines.

AIDS Dementia Complex↗
PubMed2000

NFkappaB activation, TNF-alpha expression, and apoptosis in the AIDS-Dementia-Complex.

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.

AIDS Dementia Complex↗
PubMed1990

AIDS dementia complex: brain high-energy phosphate metabolite deficits.

To test whether compromised high-energy phosphate metabolism is implicated in the neurologic impairment of acquired immunodeficiency syndrome dementia complex (ADC), brain phosphate metabolite concentrations and ratios were measured noninvasively in 12 patients with mild to moderate ADC and 29 healthy volunteers by use of localized phosphorus-31 nuclear magnetic resonance (NMR) spectroscopy and proton (hydrogen-1) magnetic resonance (MR) imaging. In patients, brain phosphocreatine (PCr) and nucleoside triphosphate (NTP) concentrations in sections through the centrum semiovale that were seen with NMR spectroscopy were reduced significantly from normal values of 4.92 mmol/kg wet weight +/- .13 (standard error of the mean) and 2.79 mmol/kg +/- .11, respectively, to 3.33 mmol/kg +/- .26 and 1.99 mmol/kg +/- .13 (P less than .0001). The ratios of metabolites detectable with P-31 NMR spectroscopy did not differ significantly from those of control subjects. The magnitude of the PCr and NTP deficits in ADC was not explicable by focal abnormalities or cerebral atrophy quantified in images of the same regions. These results are consistent with the hypothesis of a generalized virus-associated toxic process affecting brain cell function in ADC. Noninvasive measurement of metabolite concentrations with NMR spectroscopy provides new functional information that may help quantify disease progression and response to therapy.

AIDS Dementia Complex↗
PubMed1994

Cytokine circuits in brain. Implications for AIDS dementia complex.

This chapter has summarized studies showing that cells of the immune system and glial cells of the CNS use many of the same cytokines as communication signals. Activated astrocytes and microglia are the principal sources of these cytokines in the CNS, although oligodendrocytes are capable of expressing IL-1 and TGF-beta. There is a complex circuitry of interactions mediated by cytokines, especially in the event of blood-brain barrier damage and lymphoid/mononuclear cell infiltration into the CNS. Infiltrating activated macrophages produce cytokines such as IL-1, TNF-alpha, and IL-6, which would trigger glial cells to produce their own cytokines. The activation of astrocytes and microglia to secrete proinflammatory cytokines such as IL-1, TNF-alpha, IL-6, and GM-CsF may contribute to the propagation of intracerebral immune and inflammatory responses initiated by immune cells, as well as enhancement of HIV-1 expression in the CNS. The cytokine cascades ongoing in the CNS could ultimately be suppressed due to the presence of immunosuppressive cytokines such as TGF-beta. Whether immune and inflammatory responses within the CNS are propagated or suppressed depends on a number of parameters, including (a) the activational status of these cells, (b) cytokine receptor levels on glial and immune cells, (c) the presence of cytokines with both immune-enhancing and immune-suppressing effects (IFN-gamma, IL-1, TNF-alpha, IL-6, TGF-beta, CsFs), (d) the concentration and location of these cytokines in the CNS, and (e) the temporal sequence in which a particular cell is exposed to numerous cytokines (see Fig. 1). The ultimate outcome of immunologic and inflammatory events in the CNS, as well as HIV expression, will be determined, in part, by an interplay of the above parameters.

AIDS Dementia Complex↗
PubMed2004

The urokinase receptor is overexpressed in the AIDS dementia complex and other neurological manifestations.

The urokinase-type plasminogen activator (uPA) and its receptor (uPAR) play an important role in extracellular matrix degradation and cell migration in the central nervous system (CNS). To investigate the role of the uPA/uPAR system in the pathophysiology of acquired immunodeficiency syndrome dementia complex (ADC), we measured soluble uPAR (suPAR) levels in cerebrospinal fluid (CSF) and plasma from human immunodeficiency virus (HIV)-1-infected patients and controls. CSF suPAR levels were significantly higher in HIV-1-infected patients than in controls and in patients with ADC or opportunistic CNS infections (CNS-OIs) than in neurologically asymptomatic patients, irrespective of HIV-1 disease stage. The highest levels of suPAR were found in patients with ADC, and among those with CNS-OIs in patients with cytomegalovirus encephalitis or cryptococcosis. Plasma suPAR levels were higher in HIV-1-infected patients than in controls and increased with HIV-1 disease stage regardless of the presence of CNS disease. In patients with ADC or CNS-OIs, CSF suPAR levels correlated with CSF HIV-1 RNA, but not with plasma suPAR concentrations. Highly active antiretroviral therapy was associated with a significant and parallel decrease of both CSF suPAR and HIV-1 RNA. In brain tissue from patients with HIV-1 encephalitis, uPAR was highly expressed by microglial and multinucleated giant cells staining positively for HIV-1. The overexpression of uPAR in the CNS of patients with ADC suggests that the uPA/uPAR system may contribute to the tissue injury and neuronal damage in this disease.

AIDS Dementia Complex↗
PubMed1995

AIDS dementia complex: evaluation with proton MR spectroscopic imaging.

PURPOSE: To investigate cerebral metabolic changes in acquired immunodeficiency syndrome dementia complex (ADC) with proton magnetic resonance (MR) spectroscopic imaging and compare the findings with those of conventional MR imaging. MATERIALS AND METHODS: Seven patients with ADC (all men; age range, 33-58 years; mean, 43 years) with human immunodeficiency virus (HIV) infection and seven age-matched volunteers without HIV infection underwent spectroscopic and conventional MR imaging. RESULTS: Patient spectra were characterized by reduced levels of N-acetyl aspartate and increased levels of choline in white-matter regions. Lactate was detected in the cerebrospinal fluid of five patients. Four patients with mild to moderate dementia had more extensive metabolic abnormalities than three patients with only mild neurocognitive changes. CONCLUSION: Proton MR spectroscopic imaging shows extensive metabolic changes and is more sensitive than conventional MR imaging in the detection of central nervous system involvement in ADC.

AIDS Dementia Complex↗
PubMed1987

HIV antigen in the brains of patients with the AIDS dementia complex.

Human immunodeficiency virus infection was identified immunohistochemically in the brains of 8 patients with acquired immune deficiency syndrome dementia complex. Using a monoclonal antibody against a structural viral protein (p25), infection was detected in white matter and basal ganglia in a distribution paralleling that of the major neuropathological abnormalities. Viral antigen was identified principally in perivascular and parenchymal macrophages and in multinucleated cells of macrophage origin that were identified morphologically and by immunocytochemical staining for acid phosphatase isozyme. In 4 of the 8 patients, viral antigen was also detected in acid-phosphatase-negative, process-bearing neuroglial cells; in 2 patients, antigen was detected in basal ganglion cells that were morphologically consistent with neurons and in alkaline-phosphatase-positive cells with elongated nuclei that were most likely of endothelial origin.

Acquired Immunodeficiency Syndrome↗
PubMed1988

AIDS dementia complex.

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Acquired Immunodeficiency Syndrome↗
PubMed1989

Usefulness of computerized electroencephalography in diagnosing, staging and monitoring AIDS-dementia complex.

One hundred and one subjects, with various degrees of HIV infection, were enrolled in a longitudinal study aimed at evaluating the correlation between clinical and instrumental findings in the development of HIV-related subacute encephalitis. The method used was electroencephalography coupled with computerized spectral analysis (EEG-CSA) and mapping. The findings recorded by this method were compared with those obtained by computed tomography (CT) scan and neurological examination. The EEG-CSA findings were divided into four categories according to their severity. EEG-CSA was shown to be very sensitive in detecting the first signs of a forthcoming neurological disease. Following 11 months of observation, 22 out of 40 (55%) neurologically asymptomatic individuals who, at the beginning of the study showed some EEG-CSA abnormalities, had clinical evidence of a subacute encephalitis whereas only two out of 37 (5.4%) subjects who were previously free of EEG-CSA abnormalities had some signs of neurological disease (P less than 0.001) after the same period. Of those remaining who were already symptomatic when the study started, the neurological progression of HIV infection was also monitored by EEG-CSA.

Acquired Immunodeficiency Syndrome↗
PubMed1988

AIDS dementia complex.

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Acquired Immunodeficiency Syndrome↗
PubMed1997

Endocrine modulation of the neurotoxicity of gp120: implications for AIDS-related dementia complex.

HIV infection often involves the development of AIDS-related dementia complex, a variety of neurologic, neuropsychologic, and neuropathologic impairments. A possible contributor to AIDS-related dementia complex is the HIV envelope glycoprotein gp120, which damages neurons via a complex glutamate receptor- and calcium-dependent cascade. We demonstrate an endocrine modulation of the deleterious effects of gp120 in primary hippocampal and cortical cultures. Specifically, we observe that gp120-induced calcium mobilization and neurotoxicity are exacerbated by glucocorticoids, the adrenal steroids secreted during stress. Importantly, this deleterious synergy can occur between gp120 and synthetic glucocorticoids (such as prednisone or dexamethasone) that are used clinically in high concentrations to treat severe cases of the Pneumocystis carinii pneumonia typical of HIV infection. Conversely, we also observe that estradiol protects neurons from the deleterious actions of gp120, reducing toxicity and calcium mobilization.

AIDS Dementia Complex↗