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PubMed1999

Changes to AIDS dementia complex in the era of highly active antiretroviral therapy.

OBJECTIVES: To determine the protective efficacy of highly active antiretroviral therapy (HAART) against AIDS dementia complex (ADC) relative to other initial AIDS-defining illnesses (ADIs), Australian AIDS notification data over recent years were examined. METHODS: All initial ADIs in Australia over the period 1992-1997 were included. Three initial ADI groups were established: ADC; other predominantly central nervous system (CNS) ADIs (toxoplasmosis and cryptococcosis); and non-CNS ADIs. For each ADI grouping, the proportion of total ADls, and median CD4 cell count in the pre-HAART era (1992-1995) were compared with the HAART era (1996 and 1997). RESULTS: Initial ADls peaked in Australia in 1994 (n = 1049), with a gradual decline to 1996 (n = 722), and a marked decline in 1997 (n = 367). ADC constituted 4.4% of initial ADIs over the period 1992-1995, but increased after the introduction of HAART to 6.0% in 1996 and 6.5% in 1997 (P = 0.02). In contrast, the proportion of other CNS ADIs (1992-1995, 8.1%; 1996, 6.0%; 1997, 8.2%; P = 0.41) was stable over the period 1992-1997. The median CD4 cell count at ADC diagnosis increased from 70/mm3 in 1992-1995 to 120/mm3 in 1996 and 170/mm3 in 1997 (P = 0.04). Although the median CD4 cell count also increased significantly over this period for both other CNS ADIs (40-60/mm3; P = 0.02), and non-CNS ADIs (60-70/mm3; P = 0.02), the increase was small. CONCLUSION: A proportional increase in ADC compared with other ADIs and a marked increase in the median CD4 cell count at ADC diagnosis have occurred since the introduction of HAART in Australia. These changes suggest that HAART has a lesser impact on ADC than on other ADIs, with the poor CNS penetration of many antiretroviral agents a possible explanation.

AIDS Dementia Complex↗
PubMed1992

A comparison of brain perfusion SPECT in cocaine abuse and AIDS dementia complex.

Intravenous drug use is a major risk factor for HIV-1 infection. Since both AIDS dementia complex (ADC) and cocaine have been associated with abnormal brain perfusion imaging, we compared the scintigraphic patterns of ADC patients and cocaine polydrug users with normal control subjects using 99mTc-HMPAO SPECT. We found a high incidence of cortical defects in both ADC (100%) and cocaine-dependent (90%) subjects. In the cocaine and ADC patients, cortical defects were most frequent in the frontal, temporal and parietal lobes and occurred with similar frequency in the two populations. In both groups, the number of cortical defects per subject was higher than normal subjects (10.0 +/- 5.0 for ADC, 10.1 +/- 5.2 for cocaine and 0.7 +/- 1.5 for normal), background activity was high (a 65% and 60% incidence for ADC and cocaine, respectively), and basal ganglia involvement was frequent (40% and 65% for ADC and cocaine). We conclude that the brain perfusion pattern, while a sensitive indicator of ADC, cannot be distinguished from chronic cocaine polydrug use and caution should therefore be applied before entertaining a specific diagnosis.

AIDS Dementia Complex↗
PubMed2000

Highly active antiretroviral therapy for patients with AIDS dementia complex: effect on MR imaging findings and clinical course.

BACKGROUND AND PURPOSE: Recent studies have reported the clinical improvement in patients with AIDS treated with a combination of antiretroviral regimens. The purpose of our study was to describe the effects of highly active antiretroviral therapy on MR images in patients with HIV encephalopathy and to compare the clinical course with follow-up neuroimaging studies. METHODS: Initial and follow-up MR imaging findings are described in four patients with AIDS dementia complex at baseline and after antiretroviral therapy, and correlated with clinical and immunologic findings. RESULTS: Initial MR imaging revealed white matter signal abnormalities on long-TR images without mass effect and without enhancement on postcontrast images, consistent with HIV encephalopathy. Lesions were located in the basal ganglia and posterior fossa in two patients. All four patients showed progression of white matter disease on the first follow-up MR scan (mean, 6 months). On subsequent scans, regression was seen in three patients and stabilization of white matter disease was observed in one patient. Increases in CD4+ count and decreases in viral load below the limit of quantification were present in all patients. CONCLUSION: Although our patient population was small, the results suggest that disease regression in patients with AIDS dementia complex after treatment with highly active antiretroviral therapy can be characterized and monitored by MR imaging.

AIDS Dementia Complex↗
PubMed2005

HAART & the molecular biology of AIDS dementia complex.

The era of highly active antiretroviral therapy (HAART) has led to a considerable decline in the HIV disease progression rates and HIV-1-related opportunistic infections especially in developed countries. Unfortunately, antiretroviral treatment for almost 90 per cent of the HIV-infected population is not available because of cost concerns. Although a number of studies have shown uniform impact of HAART on disease progression, its effect on treating HIV infection of the brain and its manifestations, such as AIDS dementia complex (ADC), remains unclear. Along with the reasons why AIDS dementia complex continues to be a problem in the era of HAART, this review also discusses the changes in ADC patterns with HAART and its relevance in developing countries such as India. In addition, an overview of various biological, molecular and therapeutic aspects that may influence HIV dementia (HIV-D) is provided.

AIDS Dementia Complex↗
PubMed1995

Review of antiretroviral therapy in the prevention of HIV-related AIDS dementia complex (ADC).

Following the introduction of zidovudine, a major decline was noted in the incidence of AIDS dementia complex (ADC). Several factors point to a causal relationship. It is important now to review the evidence derived from clinical, cerebrospinal fluid (CSF) and neuropathological studies to determine whether the protective effect of zidovudine on the brain of patients with HIV infection has implications for clinical practice. It has been demonstrated in clinical studies that patients with ADC may improve with zidovudine treatment and that the development of ADC is rare in patients receiving the nucleoside analogue long term. In support of these clinical findings, CSF studies have revealed that the presence of HIV-1 p24 antigen has diagnostic value in patients with suspected ADC and that p24 antigen levels decline with zidovudine treatment. Supporting evidence has also come from neuropathological studies, which have demonstrated that zidovudine decreases HIV-specific neuropathological abnormalities. Recently, the Multicenter AIDS Cohort Study reported conflicting data which suggested that antiretroviral therapy is not protective against ADC; however, several methodological weaknesses of this study limit the general applicability of the findings and the conclusions. In view of the increasing body of evidence in support of the efficacy of zidovudine in the prevention and management of ADC in patients with HIV-1 infection, it seems reasonable to include this antiretroviral agent in any combination treatment regimen. Many questions remain to be answered, however, before management of such patients is optimised. Meanwhile, in order to increase both insight and evidence, it is imperative that ongoing and future clinical trials with antiretroviral drugs closely monitor all cases of progression to ADC.(ABSTRACT TRUNCATED AT 250 WORDS)

AIDS Dementia Complex↗
PubMed2005

Involvement of quinolinic acid in AIDS dementia complex.

Human immunodeficiency virus (HIV) infection is often complicated by the development of acquired immunodeficiency syndrome (AIDS) dementia complex (ADC). Quinolinic acid (QUIN) is an end product of tryptophan, metabolized through the kynurenine pathway (KP) that can act as an endogenous brain excitotoxin when produced and released by activated macrophages/microglia, the very cells that are prominent in the pathogenesis of ADC. This review examines QUIN's involvement in the features of ADC and its role in pathogenesis. We then synthesize these findings into a hypothetical model for the role played by QUIN in ADC, and discuss the implications of this model for ADC and other inflammatory brain diseases.

AIDS Dementia Complex↗
PubMed1993

Computer-based neuropsychological screening for AIDS dementia complex.

OBJECTIVE: To test the efficacy of reaction time (RT) measures as a screening test for AIDS dementia complex (ADC). DESIGN AND METHODS: Forty-two patients with mild-to-moderate ADC and 33 healthy HIV-1-seronegative control subjects took a computer-administered battery of four RT measures: simple RT, choice RT, and two types of sequential RT (1 and 2). RESULTS: The performance of the ADC group was significantly worse than that of the control group on all four RT measures, but not all tasks were equally sensitive. The two tests of sequential RT were found to be the best discriminators, and receiver operating characteristic curves analyses indicated that the optimal cut-off z score was 1.0 for both tests. CONCLUSIONS: These preliminary results suggest that computer-based RT, using these two measures of sequential RT, may provide a sensitive method of detecting HIV-1-associated cognitive deficits.

AIDS Dementia Complex↗
PubMed2003

Marked improvement in survival following AIDS dementia complex in the era of highly active antiretroviral therapy.

OBJECTIVE: To determine the effect of introduction of highly active antiretroviral therapy (HAART) on survival following AIDS dementia complex (ADC). METHODS: Australian AIDS notification data in the period 1993-2000 were examined. In order to examine the impact of HAART, two periods of AIDS diagnoses were chosen: pre-HAART (1993-1995) and HAART (1996-2000). Median survival was based on Kaplan-Meier estimates, with examination of factors influencing survival in a Cox proportional hazards model. RESULTS: In the period 1993-2000 in Australia, 5017 initial AIDS illnesses were diagnosed among 4351 AIDS patients. The proportion of AIDS cases with ADC increased from 5.2% in 1993-1995 to 6.8% in 1996-2000 (P = 0.029). Median survival following AIDS increased from 19.6 months for those diagnosed with AIDS in 1993-1995 to 39.6 months for those diagnosed in 1996-2000 (P < 0.0005). Median survival following ADC increased to a greater extent than that for all other AIDS illnesses, from 11.9 months in 1993-1995 to 48.2 in 1996-2000 (P < 0.0005). Most striking was the increase in survival among those with ADC and a CD4 cell count < 100 x 10(6) cells/l at diagnosis; 5.1 months in 1993-1995 to 38.5 months in 1996-2000 (P < 0.0005). CONCLUSION: Although there has been a proportional increase in ADC at AIDS diagnosis, survival following ADC has improved markedly in the era of HAART.

AIDS Dementia Complex↗
PubMed1992

Cerebrospinal fluid myelin basic protein as predictive marker of demyelination in AIDS dementia complex.

Myelin basic protein (MBP) was measured in cerebrospinal fluid (CSF) of patients with acquired immunodeficiency syndrome (AIDS) dementia complex (ADC) in order to investigate the degree of white matter destruction. Results show that increased CSF levels of MBP were detected in all patients with severe ADC (10/10) and, less often, in subjects with mild (2/7) or moderate dementia (7/16). No evidence of MBP-elevated concentration was observed in 14 human immunodeficiency virus (HIV)-seropositive subjects without neurological disorders and in nine HIV-seronegative controls. Our findings suggest that the measurement of CSF MBP concentration may represent a predictive marker of myelin injury and neurologic damage during the course of ADC.

AIDS Dementia Complex↗
PubMed1993

Reversal of apparent AIDS dementia complex following treatment with vitamin B12.

The human immunodeficiency virus (HIV)-associated dementia complex is characterized by difficulties in concentration and memory followed by apathy, social withdrawal and motor dysfunction. Decreased serum vitamin B12 levels occur in up to 20% of patients with acquired immune deficiency syndrome (AIDS) and may adversely contribute to the haematologic and neurologic dysfunction which is frequently attributed to the human immunodeficiency virus. We describe a patient with AIDS who presented with an apparent advanced AIDS dementia complex. There was an associated low serum vitamin B12 resulting from malabsorption due to low gastric intrinsic factor secretion. Following treatment with vitamin B12 the symptoms resolved over a 2-month period. We believe that the AIDS dementia complex represented a reversible adverse synergistic interaction between the human immunodeficiency virus and vitamin B12 deficiency.

AIDS Dementia Complex↗
PubMed2001

Varied tropism of HIV-1 isolates derived from different regions of adult brain cortex discriminate between patients with and without AIDS dementia complex (ADC): evidence for neurotropic HIV variants.

A number of infected individuals develop neuropathological disorders, such as AIDS dementia complex (ADC), as a consequence of HIV/AIDS. The biological features governing HIV entry and tropism in different brain cell types remain unclear, as do the genetics of the virus regulating these events and the neuropathogenic processes within the brain tissues. HIV-1 was isolated from the right and left parietal, occipital, and frontal lobes of the brain cortex of three HIV-1-infected patients: two with ADC and one without. The viral strains were studied from the innate tissues and various primary cell cultures. The kinetics and tropism of viral strains from different brain regions showed clear differences on various primary cell types (monocytes, monocyte-derived macrophages, and T cells), which could discriminate between biological behavior of HIV-1 strains from patients with and without ADC. The variable effect of different donor cells on tropism was also clearly evident. The majority (with a few exceptions) of isolates from different brain regions of all three patients used CCR5 as coreceptor for entry. The consistent CCR5 use, macrophage tropism, and non-syncytium-inducing phenotype were the main characteristics of the brain-derived HIV-1 strains from all three patients. Importantly, viral strains derived directly from innate brain tissue of the patient without ADC showed some differences from the cultured variants of the same patient, whereas those from brain tissue of the patients with ADC were more similar to the culture-adapted strains. This suggests that the emergence of primary cell type-adapted isolates during ADC may play a crucial role in the development and progression of the neuropathology associated with ADC. The different genotypes residing in different areas of brain combined with their differential tropism and coreceptor use suggest that neurotropic variants exist that may be governing the neurological manifestation of HIV disease in infected patients.

AIDS Dementia Complex↗
PubMed1989

Reversal of brain metabolic abnormalities following treatment of AIDS dementia complex with 3'-azido-2',3'-dideoxythymidine (AZT, zidovudine): a PET-FDG study.

Brain glucose metabolism was evaluated in four patients with acquired immunodeficiency syndrome (AIDS) dementia complex using [18F]fluorodeoxyglucose (FDG) and positron emission tomography (PET) scans at the beginning of therapy with 3'-azido-2',3'-dideoxythymidine (AZT, zidovudine), and later in the course of therapy. In two patients, baseline, large focal cortical abnormalities of glucose utilization were reversed during the course of therapy. In the other two patients, the initial PET study did not reveal pronounced focal alterations, while the post-treatment scans showed markedly increased cortical glucose metabolism. The improved cortical glucose utilization was accompanied in all patients by immunologic and neurologic improvement. PET-FDG studies can detect cortical metabolic abnormalities associated with AIDS dementia complex, and may be used to monitor the metabolic improvement in response to AZT treatment.

Acquired Immunodeficiency Syndrome↗
PubMed1996

Predictive markers of AIDS dementia complex: CD4 cell count and cerebrospinal fluid concentrations of beta 2-microglobulin and neopterin.

A predictive marker for AIDS dementia complex (ADC) in a cohort of neurologically asymptomatic human immunodeficiency virus type 1 (HIV-1)-infected patients with < 200 CD4 cells/microL was sought. Patients were assessed neurologically and neuropsychologically at entry. Blood and cerebrospinal fluid (CSF) were taken for assay of beta 2-microglobulin (beta 2M), and neopterin and T cell subsets were assessed from blood. Patients were evaluated every 4 months. Of 37 patients recruited, 35 had sufficient follow-up data. Seventeen patients progressed to ADC stage > or = 1. In univariate analyses, concentrations of CSF beta 2M and neopterin and CD4 cell count were each significantly associated with ADC development. In a multivariate analysis, concentrations of CSF beta 2M remained significant, with levels > 5 mg/L carrying approximately 17 times the risk of ADC. CSF beta 2M and neopterin levels and CD4 cell count are useful in identifying patients at risk of ADC and as such can be used to target high-risk patients so therapy can be optimized.

AIDS Dementia Complex↗
PubMed1996

High levels of anti-HIV-1 envelope antibodies in cerebrospinal fluid as compared to serum from patients with AIDS dementia complex.

The antibody response to the HIV-1 envelope protein has not been well characterized in patients with AIDS dementia complex (ADC). We evaluated the frequency of antibodies against the HIV-1 envelope in cerebrospinal fluid (CSF) and serum from 21 persons with ADC and 10 symptom-free HIV-1-positive subjects using Western immunoblot with reducing and nonreducing buffer and radioimmunoprecipitation (RIP) analysis. RIP analysis revealed anti-envelope antibodies in all sera tested. Higher anti-envelope levels were observed in CSF than in serum of 12 of 21 ADC patients and only 1 of 10 symptom-free subjects (two-sided Fisher exact test, p < 0.05). All persons with moderate to severe ADC had higher anti-envelope levels in CSF than in sera (p < 0.005). CSF anti-gp120 antibodies were not as readily detected by Western blot analysis even under nonreduced conditions, suggesting that they are directed to conformational epitopes. Higher CSF anti-envelope antibodies appear to be more common in patients with ADC than in symptom-free HIV-1-positive subjects. This antibody pattern may serve as a marker for ADC and its progression.

AIDS Dementia Complex↗
PubMed1997

Transient infection of astrocytes with HIV-1 primary isolates derived from patients with and without AIDS dementia complex.

We have studied the replication capacity of primary HIV-1 isolates obtained from four AIDS patients in astrocytes. Two patients (P1 and P2) had neurological manifestations without AIDS Dementia Complex (ADC). The other two patients (P3 and P4) had ADC. Two astrocytoma cell lines and normal fetal astrocytes were inoculated with each of these four viral isolates. Viral DNA and mRNA synthesis and also protein accumulation were followed at various times after infection. We found that tumoral as well as fetal astrocytes were susceptible to HIV-1 infection. Three of four viral isolates (P2, P3, P4) were able to infect astrocytes. Both ADC viral isolates (P3, P4) infected astrocytes with identical transcriptional patterns: rev, nef and unspliced mRNAs were expressed for 2 days after infection. The non-ADC patient (P2) with the isolate leading to viral replication in astrocytes had an HIV-1 associated multifocal demyelinating neuropathy. In this case, only nef and unspliced mRNAs were detected a few days after virus inoculation. In all cases, infection of astrocytes was transient and the level of unspliced mRNAs in infected astrocytes was lower than in chronically HIV-1 infected T cells. More extensive work would allow a better understanding of the role of astrocytes in ADC.

AIDS Dementia Complex↗