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 307 records · Page 17Linked to original sources
PubMed1998

HIV-1-infection in the CNS. A pathogenesis of some neurological syndromes in the light of recent investigations.

The main factors in the pathogenesis of AIDS-dementia complex (ADC) are analyzed. The author suggests that these factors can be divided into two groups. The "nonspecific" factors present in every immunologic processes manifested by inflammation compose the first group. They are cytotoxic lymphocytes T, the immunoactivation of infected macrophages, cytokines, NO, NOS and iNOS, the increase of the BBB permeability, the accumulation of beta-amyloid precursor protein, excitotoxic amino acids, various and numerous cells adhesion molecules. The second group may contain factors connected with HIV-1 infection of CNS. In the pathogenesis of AIDS an important role is played by toxic glycoproteins gp 120 and gp 41 which are in the coat of HIV-1 virus, nucleotide sequences variability, possibility of various virus replication in various parts of CNS, the participation of lymphokines IL-4 and IL-10, and presence of co-receptors to HIV-1 virus on lymphocytes, macrophages, neurons and microglial cells.

AIDS Dementia Complex↗
PubMed1996

Pilot Study of Didanosine in Patients with HIV Dementia.

In a pilot open-labeled study 10 subjects with AIDS dementia complex (ADC) were treated with didanosine. Only half of the subjects were able to complete the trial as a result of side effects. Five subjects exhibited improved performance on neuropsychological testing, but the mean change in performance in this small group was not statistically significant. The study suggests that this drug may have some value in ADC patients unable to tolerate other therapies, but that further study is needed to establish this firmly.

AIDS Dementia Complex↗
PubMed1998

High human immunodeficiency virus type 1 RNA load in the cerebrospinal fluid from patients with lymphocytic meningitis.

Thirty-seven matched cerebrospinal fluid (CSF) and plasma samples from 34 human immunodeficiency virus type 1 (HIV-1)-infected patients with suspected meningitis were analyzed for levels of HIV-1 RNA and markers of inflammation. Patients with tuberculous (n = 9) or cryptococcal (n = 6) meningitis had the highest CSF virus loads, which in many cases exceeded the levels in plasma, compared with patients with meningococcal meningitis (n = 3), aseptic meningitis (n = 8), tuberculoma (n = 2), or AIDS dementia complex (n = 4) or with normal lumbar punctures (n = 3). CSF virus load correlated significantly with the number of infiltrating lymphocytes (r = .60, P < .001) but not with plasma virus load, the levels of beta2-microglobulin in the CSF, or the integrity of the blood-brain barrier. These data suggest significant intrathecal HIV-1 replication in patients with lymphocytic meningeal infections such as tuberculous and cryptococcal meningitis.

AIDS Dementia Complex↗
PubMed1995

Neurologic manifestations of AIDS: a comparative study of two populations from Mexico and the United States.

Neurologic complications associated with human immunodeficiency virus type 1 (HIV-1) infection vary geographically. To understand the pattern of HIV-associated neurologic complications in Mexico, 120 AIDS patients from Mexico City, Mexico, and 500 AIDS patients from Houston, Texas, were studied cross-sectionally and retrospectively. Neurologic, laboratory, imaging, and pathologic examinations identified 40 Mexican patients and 130 U.S. patients with neurologic complications. Whereas AIDS dementia complex was the most common neurologic manifestation in both groups, intracranial tuberculoma was present only in the Mexican population (10%). Primary brain lymphoma was more prevalent in the U.S. population (8.4%). The different findings in the Mexican population likely reflect afflictions common to developing countries--a high prevalence of tuberculosis and a high mortality rate. These conditions preclude complications such as lymphoma, which develop later in the natural course of HIV infection.

AIDS Dementia Complex↗
PubMed1995

TNF-alpha- and IFN-gamma-mediated signal transduction pathways: effects on glial cell gene expression and function.

Cytokines are a group of secreted proteins that display diverse biological activity. They are especially important in the body's response to injury. They subserve a variety of both autocrine and paracrine functions by activating numerous intracellular second-messenger signaling pathways. Cytokines are known to mediate many inflammatory processes, and the inappropriate presence of cytokines in the central nervous system (CNS) has been implicated in a number of disease states. This article focuses on the biological role of two cytokines, namely: tumor necrosis factor alpha (TNF-alpha), and interferon-gamma (IFN-gamma), in the progression of neurologic disorders such as multiple sclerosis (MS) and AIDS dementia complex (ADC), with an emphasis on cytokine effects on glial cells. We discuss the cellular source of each cytokine within the CNS, their receptors, and what signaling pathways are involved in mediating their actions. We also describe recent findings indicating that HIV viral proteins, i.e., gp120, can activate cells of the CNS in a comparable manner as cytokines, and discuss the second messengers that mediate gp120-induced responses. We conclude by identifying potentially important areas of cytokine research in the context of neurologic disease.

AIDS Dementia Complex↗
PubMed1990

Dementia & depression in persons with AIDS: causes and care.

1. Nurses who care for AIDS patients are challenged to effectively manage two common problems: AIDS dementia complex (ADC) and depression. 2. Nurses can briefly assess certain neuropsychological functions related to ADC and differentiate dementia from depression. 3. Nursing interventions to manage the behaviors associated with ADC and depression can ensure patients' safety and promote the quality of their lives.

AIDS Dementia Complex↗
PubMed1992

The neurological features of HIV-positive patients in Glasgow--a retrospective study of 90 cases.

A retrospective study of the neurological problems arising in HIV-I seropositive patients in a single defined geographical area was undertaken. Ninety patients were referred for a neurological opinion from a total known HIV-I seropositive population of 436. Minor problems were frequently encountered early in the course of disease (20 at CDC stage II, 12 at CDC stage III), including seizures related to drug abuse in six. The most frequent neurological problem in those patients in CDC group IV (58 patients) were the AIDS dementia complex (14 patients), an axonal sensorimotor neuropathy (12), toxoplasmosis (nine) and cryptococcal meningitis (three). All patients with a structural lesion had appropriate focal signs on examination. The value and role of CT cranial scanning in the diagnosis of toxoplasmosis is discussed and the importance of recognizing potentially treatable causes of both intellectual impairment and cytomegalovirus-related neuropathies is stressed. This is the first report of an unselected series of patients at all stages of HIV-I related neurological disease from a single UK centre.

AIDS Dementia Complex↗
PubMed1997

Infection of macaque monkeys with simian immunodeficiency virus: an animal model for neuro-AIDS.

Due to the worldwide AIDS pandemic, HIV-1 has become the major factor for central nervous system (CNS) diseases. Two major disorders of the CNS caused by HIV-1 have been described, a meningoencephalitis which occurs in 30-50% of patients early after infection and the AIDS dementia complex (ADC, also known as HIV-associated dementia) which is characterized by a predominantly subcortical dementia. The pathophysiology of these clinical syndromes still remains an enigma. However, since monocytes/macrophages may represent the major place of virus replication in the CNS, a hematogenous invasion of HIV-1 into the brain may be crucial to the neuropathogenesis of ADC. One of the most valuable animal models for the study of neuro-AIDS is the infection of macaque monkeys with the simian immunodeficiency virus (SIV). In about 50% of infected rhesus monkeys with an AIDS-like disease, neuropathological lesions similar to ADC in men have been observed. This animal model contributes to our understanding of the mechanisms of viral neuroinvasion early after infection and in the development of neurological disease. In this review we will summarize the state of the art and will focus on further questions concerning the neuropathogenesis of HIV/SIV.

AIDS Dementia Complex↗
PubMedDate not supplied

Neurologic and psychiatric manifestations of HIV disease.

Neuropsychiatric problems have assumed an increasingly prominent role in HIV-infected individuals. Disease occurs at all levels of the central and peripheral nervous systems by a variety of mechanisms. The AIDS dementia complex is the prototypical example of "direct" effects of HIV on the neuraxis, while infections such as toxoplasmosis and cryptococcal meningitis are complications of HIV-induced immunosuppression. Neurologic manifestations vary in frequency depending upon the overall stage of HIV disease; diagnostic difficulties may be encountered because of HIV's effect on cerebrospinal fluid parameters. The uncertainties of management of neurosyphilis in this setting provide and example of these problems. As is the case with other organ systems, the main goal of neurodiagnostic efforts is to find the increasing number of treatable components of neuropsychiatric dysfunction.

AIDS Dementia Complex↗
PubMed2002

AIDS dementia.

AIDS dementia complex is a relatively recently discovered source of cognitive and motor decline, clearly linked to CNS infection by HIV. While this condition is generally subacutely progressive, and leads to death in a short time-span in untreated patients, improvement in function and prognosis may be achieved by application of highly active antiretroviral therapy. Although this therapy is essential, it may also be necessary in the long term to provide additional neuroprotection, blocking secondary mechanisms of neurotoxicity. With current therapy, infection is never completely eradicated, and significant portions of toxicity seem mediated by indirect mechanisms that may continue even during antiretroviral therapy.

AIDS Dementia Complex↗
PubMed2000

PCR detection of host and HIV-1 sequences from archival brain tissue.

Mutations in CCR5 and CCR2b have been recently shown to affect disease progression towards AIDS. A role for these host genotypes in AIDS dementia complex (ADC) has also been postulated but remains unclear. Additionally, brain-derived envelope sequences from HIV-1 have been associated with ADC but their specific contribution to pathogenesis remains uncertain. This study demonstrates the successful use of PCR techniques to isolate host CCR5 and CCR2b, and HIV-1 V3 sequences from paraffin embedded tissues from patients with and without ADC. PCR amplification from archival tissue offers a novel approach for studying the interactions between potential neuroprotective elements in the host and virulence determinants in HIV that may contribute to differences in susceptibility to ADC.

AIDS Dementia Complex↗
PubMed1999

Lack of association between Borna disease virus infection and neurological disorders among HIV-infected individuals.

Viruses have been proposed as etiologic cofactors in the pathogenesis of HIV-related neurological disease. To investigate the etiologic potential of Borna disease virus (BDV) in these disorders, two populations were studied: (1) 27 prospectively identified patients with various neurological disorders were evaluated with BDV RT-PCR (CSF, PBMC), and BDV serology, and (2) a separate group of 25 retrospectively studied patients with AIDS dementia complex was evaluated using BDV serology only. A novel, BDV p40 gene RT-PCR assay was developed: conserved primers were used in a non-nested amplification, detecting less than 100 BDV RNA copies and all of nine wild-type, confirmed animal BDV infections. BDV seroprevalences were 12.5% and 8.0%, respectively, which are similar to the general HIV-infected population. None of the prospectively studied patients had detectable BDV RNA in their CSF or PBMC. Our findings do not support the hypothesis that BDV infections are responsible for HIV-related neurological disorders.

AIDS Dementia Complex↗
PubMed2004

Prevalence and pattern of neuropsychological impairment in human immunodeficiency virus-infected/acquired immunodeficiency syndrome (HIV/AIDS) patients across pre- and post-highly active antiretroviral therapy eras: a combined study of two cohorts.

The objective of this study was to assess the prevalence and pattern of neuropsychological impairment in cohorts of human immunodeficiency virus (HIV)-infected individuals across pre- and post-HAART (highly active antiretroviral therapy) eras. Two cohorts of HIV-infected individuals attending tertiary referral hospital outpatient clinics were studied. The cohorts represented two eras of antiretroviral medication: monotherapy (n = 51) and HAART (n = 90). Each was compared in nine neuropsychological domains in regard to the prevalence as well as pattern of neuropsychological impairment. Because the authors intended to characterize the prevalence and pattern of neuropsychological deficits in nondemented advanced HIV-infected individuals, patients with a current diagnosis of acquired immunodeficiency syndrome (AIDS) dementia complex were not included. The prevalence of impairment was not significantly different across pre-HAART and HAART eras using a standard criterion to define impairment: -2 SD in two neuropsychological measures (41.1%/38.8%). Prevalence of deficits was not significantly reduced in patients with undetectable plasma viral load. The pattern of neuropsychological impairment was different across pre-HAART and HAART eras, with an improvement in attention, verbal fluency, visuoconstruction deficits, but a deterioration in learning efficiency and complex attention. This change remained even in patients with an undetectable plasma viral load, although the severity was partially diminished. Neuropsychological deficits remain common in the HAART era, essentially uninfluenced by HAART. The finding that some neuropsychological functions are improving while other are deteriorating indicates that these deficits do not reflect "burnt out" damage but rather that there is an active intracerebral process occurring, the nature of which is still to be determined.

AIDS Dementia Complex↗
PubMed1992

Tumour necrosis factor (TNF-alpha) and neurological disorders in HIV infection.

Tumour necrosis factor (TNF-alpha) concentrations were determined in the CSF from 42 HIV-infected patients, with or without CNS involvement. In addition, 14 subjects with various neurological disorders but without HIV antibodies were included as controls. Raised CSF concentrations of TNF-alpha (greater than 40 ng/l) were detected both in patients with AIDS dementia complex (ADC) (6/9) and with CNS opportunistic infections (10/19) and, less commonly, in HIV infected subjects without CNS diseases (2/14) and in anti-HIV negative controls (1/14). The highest CSF concentrations of TNF-alpha (greater than 100 ng/l), however, were found in seven out of eight patients with cryptococcal meningitis. Although a role for TNF-alpha in demyelinating lesions associated with ADC has been suggested, our results indicate that a clear elevation of TNF-alpha in the CSF from HIV positive patients mostly occurs in acute inflammatory disorders, such as cryptococcal meningitis.

AIDS Dementia Complex↗
PubMed1998

[Risk of the development of dementia after interruption of zidovudine treatment].

BACKGROUND: Epidemiologic data suggest that zidovudine (ZDV) could prevent the AIDS dementia complex (ADC), but this hypothesis has been specifically studied. PATIENTS AND METHODS: We have reviewed the medical records of all patients with human immunodeficiency virus (HIV) infection admitted to our section between January 1990 and December 1993 who were diagnosed with ADC, and we have compared them to those of a control group with regard to the interruption of ZDV at least 3 months before. Controls were selected from the remaining HIV-related admissions, matched by calendar year, CD4-cell count and previous HIV-disease stage. RESULTS: Thirty-nine cases and 39 controls were available for analysis; twenty-nine (74%) and 25 (64%) were male. The median age was similar for both groups: 30. Thirty-one patients (79%) in each group had a previous diagnosis of AIDS, six (15%) in each group had an AIDS-related complex and in two (5%) the ADC was the first complication of their HIV disease. The median CD4-cell counts were 79.6 and 79.4 x 10(6)/l. Twenty-three patients in each group had taken ZDV. Six of these from the ADC had withdrawn treatment, as compared to 2 from the control group (odds ratio [OR] 3.36; 95% confidence interval [CI]: 0.54-35.76). On the other hand, 16 patients with ADC were still on ZDV at the time of diagnosis, as compared to 21 controls (OR: 0.66; 95% CI: 0.22-1.60). CONCLUSION: In this case-control study, the interruption of treatment with ZDV was not found to be a risk factor for the development of ADC.

AIDS Dementia Complex↗
PubMed1991

Molecular characterization of human immunodeficiency virus type 1 cloned directly from uncultured human brain tissue: identification of replication-competent and -defective viral genomes.

All presently available replication-competent proviral clones of human immunodeficiency virus type 1 (HIV-1) are derived from cell culture-amplified virus. Since tissue culture is highly selective for viral strains with an in vitro growth advantage, such clones may not be representative of the biologically relevant virus present in vivo. In this study, we report the molecular cloning and genotypic characterization of 10 HIV-1 genomes directly from uncultured brain tissue of a patient with AIDS dementia complex. Targeting unintegrated circular HIV-1 molecules for recombinant lambda phage cloning, we obtained four full-length genomes with one or two long terminal repeats (LTRs), three defective genomes with internal deletions, two rearranged genomes with inverted LTR sequences, and one integrated proviral half with flanking cellular sequences. Nucleotide sequence analysis of these clones demonstrated chromosomal integration, circle formation, genomic inversion, and LTR-mediated autointegration of HIV-1 genomes in vivo. Comparison of a 510-bp hypervariable envelope region among 8 lambda phage-derived and 12 polymerase chain reaction-derived clones from the same brain specimen identified a predominant viral form as well as genetically divergent variants. Variability among 19 of 20 clones ranged between 0.2 and 1.2%. One clone exhibited 8.2% nucleotide sequence differences consisting almost exclusively of G-to-A changes. Transfection of the four full-length HIV-1 genomes identified one clone (YU-2) as replication competent and exhibiting growth characteristics similar to those of tissue culture-derived macrophage tropic strains of HIV-1. These results demonstrate, for the first time, that replication-competent HIV-1 genomes, complex mixtures of defective viral forms, and chromosomally integrated provirus persist in vivo. In addition, the brain-derived viral clones are expected to prove valuable for future studies of macrophage and neurotropism as well as for the analysis of other viral properties that are subject to in vitro selection pressures.

AIDS Dementia Complex↗
PubMed1994

[Paranoid hallucinatory psychoses as the first manifestation of HIV infection].

All parts of the central nervous system may be involved in HIV infection, resulting in a variety of neuropsychiatric syndromes some of which resemble functional psychoses. Corresponding to the HIV-associated disease these syndromes differ in course and severity. A very common form is the AIDS-dementia complex, especially late in the course of disease. Up to now, however, a specific therapy is not available. A case of severe psychosis with paranoid delusions and hallucinations in a patient with otherwise asymptomatic HIV infection is reported. From her biography it was concluded that the infection occurred 10 years earlier. During therapy with azidothymidine, symptoms disappeared within 3 months, and more than one year after admission to our hospital the patient was still able to work. According to the course of the disease in this patient, reports from the literature and pathogenetic theories, an early therapy with antiviral agents is recommended in HIV-induced subacute encephalitis.

AIDS Dementia Complex↗
PubMed2001

Crosstalk between components of the blood brain barrier and cells of the CNS in microglial activation in AIDS.

During the progression of AIDS, a majority of patients develop cognitive disorders such as HIV encephalitis (HIVE) and AIDS dementia complex (ADC), which correlate closely with macrophage infiltration into the brain and microglial activation. Microglial activation occurs in response to infection, inflammation and neurological disorders including HIVE, Alzheimer's disease, Parkinson's disease and multiple sclerosis. Microglia can be activated by immunoreactive cells independent of, but enhanced by HIV infection, from at least two routes. Activation may occur from signals originating from activated monocytes and lymphocytes in the blood stream, which initiate a cascade of stimuli that ultimately reach microglia in the brain or from activated macrophages/microglia/astrocytes within the brain. Effects of microglial activation stemming from both systemic and CNS HIV infection act together to commence signaling feedback, leading to HIVE and increased neurodegeneration. Most recent data indicate that in AIDS patients, microglial activation in the brain with subsequent release of excitotoxins, cytokines and chemokines leads to neurodegeneration and cognitive impairment. Since the presence of HIV in the brain results from migration of infected monocytes and lymphocytes across the vascular boundary, the development of novel therapies aimed at protecting the integrity of the blood brain barrier (BBB) upon systemic HIV infection is critical for controlling CNS infection.

AIDS Dementia Complex↗