Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “AIDS Dementia Complex”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 217 records · Page 12Linked to original sources
PubMed1993

Human immunodeficiency virus infection, dementia and the older patient.

Australian statistics have shown that 10.9% of AIDS cases have occurred in the 50 years and over age group. To date little attention has been given to the many issues surrounding HIV infection in the older population, for example, the failure to consider HIV as an aetiological factor in the older person presenting with neuropsychiatric disorder and the potential for misdiagnosis of AIDS dementia complex as dementia of the Alzheimer type. This paper includes a discussion of the clinical features of the AIDS dementia complex, its resemblance to the syndrome of "subcortical dementia", and review of the literature reporting dementia as the presenting feature of HIV infection in older individuals.

AIDS Dementia Complex↗
PubMed1995

Radionuclide brain imaging in acquired immunodeficiency syndrome (AIDS).

Infection with the human immunodeficiency virus-type 1 (HIV-1) may produce a variety of central nervous system (CNS) symptoms and signs. CNS involvement in patients with the acquired immunodeficiency syndrome (AIDS) includes AIDS dementia complex or HIV-1 associated cognitive/motor complex (widely known as HIV encephalopathy), progressive multifocal leucoencephalopathy (PML), opportunistic infections such as Toxoplasma gondii, TB, Cryptococcus and infiltration by non-Hodgkin's B cell lymphoma. High resolution structural imaging investigations, either X-ray Computed Tomography (CT scan) or Magnetic Resonance Imaging (MRI) have contributed to the understanding and definition of cerebral damage caused by HIV encephalopathy. Atrophy and mainly high signal scattered white matter abnormalities are commonly seen with MRI. PML produces focal white matter high signal abnormalities due to multiple foci of demyelination. However, using structural imaging techniques there are no reliable parameters to distinguish focal lesions due to opportunistic infection (Toxoplasma gondii abscess) from neoplasm (lymphoma infiltration). In this manuscript we review the use of radionuclide brain imaging techniques in the investigation of HIV infected patients. Brain perfusion single photon emission tomography (SPET), neuroreceptor and positron emission tomography (PET) studies are reviewed. Greater emphasis is put on the potential of some radiopharmaceuticals, considered to be brain tumor markers, to distinguish intracerebral lymphoma infiltration from Toxoplasma infection. SPET with 201Tl using quantification (tumour to nontumour radioactivity ratios) appears a very promising technique to identify intracerebral lymphoma.

AIDS Dementia Complex↗
PubMed1995

Neurocytotoxity of quinolinic acid in human brain cultures.

Quinolinic acid (QUIN) is a tryptophan metabolite which has been found to be an excitotoxin in rats, although its toxicity in humans is unknown. QUIN has been implicated in the pathogenesis of AIDS dementia complex. This study examined the effect of QUIN on human fetal brain tissue in vitro. After at least 14 days in vitro, QUIN was added to the cultures in the feeding medium, and lactate dehydrogenase (LDH) efflux at 20 h and neuronal morphology were used as a measure of neuronal injury. LDH levels in media from cultures exposed to QUIN concentrations of 5 and 10 mM were consistently elevated compared to controls. Overall, LDH levels in media from cultures exposed to lower QUIN concentrations did not differ significantly from controls. These data are comparable to animal in vitro studies, and support the hypothesis that QUIN is toxic to human central nervous system neurons and further strengthen its potential role in the pathogenesis of AIDS dementia complex.

AIDS Dementia Complex↗
PubMed1990

Abnormalities in cholesterol metabolism cause peripheral neuropathy and dementia in AIDS--a hypothesis.

The AIDS dementia complex and peripheral neuropathy in AIDS are considered to be direct or indirect manifestations of HIV infection, yet the pathogenesis in unclear. There are parallels between AIDS and Tangier disease clinically and histopathologically and in lipid metabolism. The neurological disorders in AIDS may be caused by dysfunction of cellular cholesterol transport. Substitution of high density lipoprotein is recommended in the treatment of severe polyneuropathy and dementia in AIDS.

AIDS Dementia Complex↗
PubMed2002

Antiretroviral therapy regimens for neuro-AIDS.

In the era of highly active antiretroviral therapy (HAART) the central nervous system (CNS) becomes increasingly important as a sanctuary site for the human immunodeficiency virus (HIV-1). HIV-1-associated brain disease is subdivided into the minor cognitive/motor disorder, the minor cognitive/motor complex and the AIDS dementia complex, all of which are predictive for patients' deaths. CNS effective therapy therefore influences the prognosis of each individual patient. Thus, there is urgent need both for prophylactic and therapeutic strategies preventing or treating HIV-1-associated CNS disease. HAART consisting of two nucleoside analogues (NAs), one or two protease inhibitors (PIs) and/or one non-nucleoside inhibitor of the reverse transcriptase (NNRTI) has a neuroprophylactic value with regard to the manifestation of HIV-I associated CNS disease. With regard to therapeutic effects, the NAs zidovudine and stavudine penetrate into the cerebrospinal fluid and positively influence HIV-1-associated brain disease. Adding a second NA has no additional therapeutic effect. NNRTIs (nevirapine and efavirenz) are also CNS effective. However, there is a subgroup of non-responders, who obviously need other forms of therapeutic interventions. The very few existing studies point out that patients with high plasma viral loads and neurological abnormalities should be treated with a combination of two NAs and one NNRTI. The value of PIs for CNS protection remains to be evaluated.

AIDS-Associated Nephropathy↗
PubMed2004

Serum and cerebrospinal fluid levels of interleukin-18 in human immunodeficiency virus type 1-associated central nervous system disease.

Interleukin-18 (IL-18) is a proinflammatory cytokine released by macrophages that strongly stimulates the production of interferon-gamma, thereby linking innate and acquired immunity. Its role in human immunodeficiency virus (HIV) pathogenesis is under debate and little is known about its role in neuro-AIDS (acquired immunodeficiency syndrome). Serum and cerebrospinal fluid (CSF) levels of IL-18 were determined by a commercially available enzyme-linked immunosorbent assay (ELISA) in 22 HIV-seropositive patients without neurological symptoms (HIV+), 21 patients with AIDS dementia complex (ADC), and 31 patients with AIDS-defining opportunistic infections (OIs) of the brain. Thirty-two HIV seronegative patients (HIV-) served as controls. Compared to HIV- controls, serum IL-18 levels were increased in HIV+ and ADC but not in OI patients. In contrast, CSF IL-18 levels were elevated in OI patients whereas HIV+ and ADC patients were not different from HIV- controls. We provide evidence for an significantly increased IL-18 level in the CSF of HIV+ patients with cerebral OIs, suggestive of a role for IL-18 in the intrathecal host response to OIs.

AIDS Dementia Complex↗
PubMed1998

SIV infection of macaques--modeling the progression to AIDS dementia.

AIDS dementia complex affects 15-20% of HIV-infected adults and a greater percentage of HIV-infected children. Whether or not an HIV-infected individual develops neurological disease and how early in infection the clinical signs appear is most likely the net result of both viral virulence factors and host factors. Important viral factors include cell tropism and sequences that determine neurovirulence. The host factors include the cellular expression of viral co-receptors and maintenance of competent immune responses. The pathogenesis of AIDS dementia complex is difficult to study in the human host because of the difficulty in identifying acutely infected individuals and the inaccessibility of human brain tissue for examination during infection. The SIV/macaque model is excellent for the study of viral virulence factors and host responses to infection. This review outlines how the SIV/macaque model has been used to identify viral factors that are important for the development of neurological disease, to determine when HIV enters the brain, and to characterize the host immune responses affecting virus entry to the CNS and the development of neurological disease.

AIDS Dementia Complex↗
PubMed1999

Increased cerebrospinal fluid protein tau concentration in neuro-AIDS.

OBJECTIVES: Assessment of cerebrospinal fluid (CSF) levels of protein tau in human immunodeficiency virus type 1 (HIV-1) infection. MATERIAL AND METHODS: CSF tau levels were analyzed in 52 HIV-1-infected patients, 37 of whom had no neurological symptoms, eight had aquired immunodeficiency syndrome (AIDS) dementia complex (ADC), and seven had AIDS with other neurological complications. RESULTS: A significantly higher mean CSF tau concentration was found in patients with ADC (380 pg/ml) compared with patients with neuroasymptomatic HIV-1 infection (120 pg/ml, P<0.01) and HIV-negative controls (150 pg/ml, P<0.05). No difference in CSF tau levels was found between patients with ADC and patients with AIDS with other neurological complications. CONCLUSION: CSF tau might be used as a biochemical marker for axonal degeneration and might be of use to identify HIV-1-infected patients with ADC and other neurological complications, but it cannot discriminate between ADC and other neurological complications in HIV-1-infection.

AIDS Dementia Complex↗
PubMed1997

Intrathecal reactivity for myelin components precedes development of neurological symptoms in AIDS patients.

The central nervous system is considered an early and common target for the human immunodeficiency virus type 1 (HIV-1). Serum and cerebrospinal fluid (CSF) from 20 HIV positive patients, including 14 with AIDS-dementia complex (CDC stage IV) and 6 asymptomatic individuals (CDC stage II) were analyzed by enzyme immunoassay for detection of antibodies to native myelin basic protein (MBP) and for the amino acid sequence 68-84 exposed after partial degradation of native MBP. Control groups included HIV-1 negative patients with degenerative and/or vascular dementia, chronic multiple sclerosis (MS) and individuals without any sign of neurological or cognitive disturbances. As opposed to control groups, serum and CSF samples from MS and HIV-1 infected patients showed several oligoclonal bands running in the gamma region. AIDS-dementia complex (ADC) patients had increasingly high intrathecal IgG specific antibody titers for the amino acid sequence 68-84 of MBP. Marked intrathecal antibody production for myelin components was also detected in the majority of HIV-1 infected asymptomatic individuals. Such alteration paralleled development of cognitive deficits, neurological abnormalities and appearance of CNS demyelinating plaques. Preferential immune recognition of this myelin epitope within the CSF during early stages of HIV-1 infection might point to an ongoing process of active demyelination and ultimately indicate subclinical CNS involvement.

AIDS Dementia Complex↗
PubMed1993

Cerebrospinal fluid concentration of fibronectin in patients with HIV-1 infection and central nervous system disorders.

AIMS: To evaluate the fibronectin concentrations in the cerebrospinal fluid of HIV-1 infected patients with central nervous system disorders. METHODS: Fibronectin was determined by an immunoturbidimetric assay in 41 HIV-1 infected patients with AIDS dementia complex, progressive multifocal leucoencephalopathy, and opportunistic infections. RESULTS: A significant decrease in fibronectin concentrations in the cerebrospinal fluid of patients with AIDS and dementia complex and progressive multifocal leucoencephalopathy was observed, as well as in those with opportunistic infections of the central nervous system (p < 0.0001). In particular, a significant decrease in fibronectin concentration in cerebrospinal fluid was observed in patients with cerebral toxoplasmosis and cryptococcal meningitis (p < 0.0001). CONCLUSIONS: Because fibronectin can bind to several viruses, fungi, and protozoa, it is conceivable to suppose that the consumption of fibronectin in the cerebrospinal fluid of patients with neurological disorders may be related to the binding of fibronectin to HIV itself, or to viral proteins, or to organisms responsible for opportunistic infections.

AIDS Dementia Complex↗
PubMed1997

Regulation of glutathione and cell toxicity following exposure to neurotropic substances and human immunodeficiency virus-1 in vitro.

The aim of the present study was to assess the toxic potential of drugs of abuse and other neuropharmacological agents in the pathogenesis of AIDS dementia complex (ADC), the neurological complication of AIDS. Neuroblastoma and glioblastoma cell lines expressing the dopamine transporter, as well as primary macrophages exposed to human immunodeficiency virus-1 (HIV-1), were used to investigate the possibility of any synergistic effect between the mode of toxicity of such substances and virus exposure. The drugs of abuse used in our experiments were cocaine and morphine, which exert their action, among others, on the dopaminergic system. Effects were compared to treatment with dopamine itself and a typical dopaminergic drug used pharmaceutically, selegiline. In macrophage cultures, glutathione (GSH) was upregulated strongly after treatment with dopamine, morphine or selegiline, and this effect was enhanced when cells were pre-exposed to virus. This upregulation is discussed as a compensatory reaction to an oxidative signal. When hydrogen peroxide plus iron sulfate was used as a strong oxidant in macrophages, GSH concentrations decreased as a result of cell injury. Cell numbers remained constant in all treatment groups. In contrast, in both neuroblastoma and glioblastoma cell lines, the modulation of GSH concentrations by neurotropic substances was accompanied by significant cell loss, which was exacerbated by HIV-1 pretreatment. Selegiline did not change cell numbers when incubated alone. However, when incubated following treatment with HIV-1 cell death was highly significant. Ascorbic acid (AA), included as antioxidant, totally restored cell loss in cultures treated with dopamine. However, no effect was observed in combined treatment of AA and morphine or selegiline. The results demonstrate a synergistic role in cellular toxicity due to neurotropic substances and HIV-1, and suggest that neuropharmacological agents may contribute to the pathogenesis of ADC.

AIDS Dementia Complex↗
PubMed1996

[Cerebral proton spectroscopy of people infected with the human immunodeficiency virus].

BACKGROUND: This article presents a combined magnetic resonance imaging and proton spectroscopy protocol (MRI/1H-MRS) applied to study the brain of human immunodeficiency virus (HIV) infected patients. The spectroscopic results were compared with clinical and radiological parameters. PATIENTS AND METHODS: The proton spectra of 57 HIV patients and 20 control subjects were obtained from a volume of interest of 8 cm3 located in the parietooccipital region of the brain that did not include any focal lesion. The resonance areas due to N-acetyl aspartate (NAA), creatine (Cr) and choline (Cho) were obtained. The MRI exam allowed us to determine the presence of focal or diffuse lesions and the degree of atrophy. Finally, the clinical exploration included the performance of a Mini-Mental test. The NAA/Cr, NAA/Cho and Cho/Cr ratios were correlated with clinical characteristics, the result of the Mini-Mental test, the presence of lesions and the degree of atrophy. RESULTS: There were altered spectral patterns in a volume of the brain that did not contain any focal lesion. The decrease in the NAA/Cr or NAA/Cho ratios was significative when considering the presence of atrophy, the existence of signs of cognitive deficiencies or the diagnosis of AIDS-dementia complex. CONCLUSIONS: The spectral changes found in the present study suggest the existence of neuronal lesions that would be due to the HIV-infection. A combined MRI/1H-MRS study may provide a more complete information about the neurological impairment by HIV and could constitute a marker of AIDS-dementia complex.

Adult↗
PubMed1995

Common neurologic complications of HIV-1 infection and AIDS.

Complications of human immunodeficiency virus type 1 infection and acquired immunodeficiency syndrome may involve any level of the central or peripheral nervous system. Acute encephalitis, aseptic meningitis and acute demyelinating polyneuropathy may occur early in the course of HIV infection, while dementia, central nervous system-related cancer, opportunistic infections and autonomic neuropathy typically present later. Headache and mental status changes are common early manifestations of central nervous system involvement. Most severe headaches are related to an identifiable cause, including a mass lesion, opportunistic cerebral infection and medication side effect. Memory deficits, concentration difficulties and abnormalities on mental status testing may represent early AIDS dementia complex (HIV encephalopathy), the most common neurologic complication. In patients with AIDs, the differential diagnosis of cerebral mass lesions on computed tomography or magnetic resonance imaging includes cerebral toxoplasmosis, tuberculous or fungal abscess, focal viral encephalitis, metastatic resonance imaging includes cerebral toxoplasmosis, tuberculous or fungal abscess, focal viral encephalitis, metastatic Kaposi's sarcoma and primary CNS lymphoma. Peripheral neuromuscular disease, including distal symmetric polyneuropathy, autonomic neuropathy, and HIV and chronic zidovudine myopathy, affects 15 to 40 percent of all persons with HIV infection or AIDS.

AIDS Dementia Complex↗
PubMed1989

Identification of mononuclear cells in CSF of patients with HIV infection.

Using immunocytochemical methods, CSF lymphocyte subpopulations were examined in different neurologic disorders associated with human immunodeficiency virus (HIV) infection. CSF pleocytosis was observed in asymptomatic neurologically normal subjects, in patients with aseptic meningitis, and those with inflammatory demyelinating neuropathies, but infrequently in subjects with AIDS dementia complex. The distribution of CSF lymphocyte subpopulations in HIV-infected patients differed from control subjects showing decreases in percentages of T helper (CD4) cells and increases in T suppressor (CD8) cells. Peripheral blood and CSF CD4:CD8 ratios were inverted in all of the neurologic disorders studied. In all disorders, the changes in CSF composition of mononuclear cells paralleled alterations in peripheral blood and in patients with AIDS dementia complex, there was a relationship between the severity of dementia and blood and CSF CD4 lymphocyte proportions.

Acquired Immunodeficiency Syndrome↗
PubMed1990

[AIDS and dementia].

Two case histories are presented of patients with AIDS. In both cases, the initial symptom, apart from the generalized symptoms, was rapidly progressive dementia. The most important neurological symptoms in the AIDS dementia complex are reviewed and the CNS complications of AIDS are mentioned. In patients with atypical neurological clinical pictures, the diagnosis of AIDS should be considered.

AIDS Dementia Complex↗
PubMed1995

HIV-1 gp120-induced neurotoxicity to midbrain dopamine cultures.

HIV-1-associated cognitive/motor dysfunction is a frequent neurological complication of acquired immunodeficiency syndrome (AIDS) and has been termed AIDS dementia complex (ADC). The HIV-1 envelope glycoprotein gp120 has been implicated in producing brain injury associated with ADC. The purpose of the present study was to determine if gp120-induced neurotoxicity is associated with damage to dopaminergic systems. Exposure of rat midbrain dopamine cultures to gp120 for 3 days reduced the ability of dopaminergic cells to transport this amine and also resulted in a reduction in dopamine neuron process length while it did not alter either dopamine cell number or the total number of neuronal cells. These detrimental effects of gp120 were prevented by an NMDA receptor antagonist (MK-801) or by preincubation with anti-gp120 antibody. These results suggest that dopaminergic neuronal damage may contribute to the manifestations of AIDS dementia complex.

Animals↗
PubMed1992

Spectrum of human immunodeficiency virus-associated neocortical damage.

A spectrum of neurocognitive defects, termed human immunodeficiency virus type 1 (HIV-1)-associated cognitive/motor complex, has been described in patients with acquired immunodeficiency syndrome (AIDS). AIDS dementia complex (ADC) is a severe form of this disease seen in 20 to 30% of terminally ill patients. The etiology of this complex is distinct from commonly observed opportunistic infections seen in brains of patients with AIDS and has been attributed to HIV infection within the brain. At autopsy, the brains of patients with ADC contain numerous HIV-infected macrophages/microglia with prominent subcortical damage, together termed HIV encephalitis. We retrospectively analyzed all 107 brains from a three-year period (1988-1990) of AIDS autopsies using immunocytochemistry to detect HIV. Rather than breaking into distinct groups of HIV encephalitis versus non-HIV encephalitis, the specimens revealed a spectrum of severity of HIV infection. Although only 16% of the brains showed the histological hallmarks of HIV encephalitis, more than 50% of the autopsies showed moderate to severe HIV infection. In a subset of 23 AIDS autopsies during which short postmortem times and absence of significant opportunistic infection permitted quantitative analysis of dendritic and synaptic complexities, we identified a strong correlation between neocortical dendritic and presynaptic damage and abundance of HIV envelope protein in the neocortical gray and deep white matter. This correlation suggests that the presence of HIV-1 in the neocortex may be responsible by direct or indirect mechanisms for dendritic and synaptic damage.

AIDS Dementia Complex↗
PubMed1998

Chemokine receptor expression on resident and inflammatory cells in the brain of macaques with simian immunodeficiency virus encephalitis.

Although the mechanisms of human immunodeficiency virus (HIV) neuroinvasion, neuronal injury, and subsequent development of HIV-1-associated AIDS dementia complex are not fully understood, a correlation between monocyte/macrophage infiltrates in the brain and neurological disease exists. In light of the many potential roles that chemokines and chemokine receptors may play in HIV neuropathogenesis, we sought to describe their pattern of expression in the SIV-infected rhesus macaque model of HIV encephalitis. We previously demonstrated elevated expression of the chemokines macrophage inflammatory protein (MIP)-1alpha, MIP-1beta, RANTES, and interferon-inducible protein (IP)-10 in brain of macaque monkeys with SIV encephalitis. In this study, we demonstrate that the corresponding chemokine receptors CCR3, CCR5, CXCR3, and CXCR4 are expressed in perivascular infiltrates in these same tissues. In addition, we detected CCR3, CCR5, and CXCR4 on subpopulations of large hippocampal and neocortical pyramidal neurons and on glial cells in both normal and encephalitic brain. These findings suggest that multiple chemokines and their receptors contribute to monocyte and lymphocyte recruitment to the brain in SIV encephalitis. Furthermore, the expression of known HIV/SIV co-receptors on neurons suggests a possible mechanism whereby HIV or SIV can directly interact with these cells, disrupting their normal physiological function and contributing to the pathogenesis of AIDS dementia complex.

Animals↗