aids dementia complex/protease

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Regression of HIV encephalopathy and basal ganglia signal intensity abnormality at MR imaging in patients with AIDS after the initiation of protease inhibitor therapy.

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OBJECTIVE To determine whether protease inhibitors cause regression of periventricular white matter signal intensity abnormalities in patients with human immunodeficiency virus (HIV) encephalopathy and whether the changes on magnetic resonance (MR) images correlate with cognitive

Protease inhibitors may reverse AIDS dementia.

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Trypsin inhibition: a potential cause of cobalamin deficiency common to the pathogenesis of Alzheimer-type dementia and AIDS dementia complex?

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There is increasing evidence for an association between Alzheimer-type dementia (AD) and nutritionally independent cobalamin deficiency. Furthermore, low serum cobalamin values occur in a kindred with familial Alzheimer's disease (FAD) and histopathological confirmation of AD neuropathology. The

The antiretroviral protease inhibitors indinavir and nelfinavir stimulate Mrp1-mediated GSH export from cultured brain astrocytes.

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Combinations of antiretroviral drugs are successfully used for the treatment of acquired immune deficiency syndrome and reduce the incidence of severe human immunodeficiency virus (HIV)-associated dementia. To test whether such drugs affect the GSH metabolism of brain cells, we have exposed

Failure to detect nelfinavir in the cerebrospinal fluid of HIV-1--infected patients with and without AIDS dementia complex.

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OBJECTIVE To assess the penetration of the HIV-1 protease inhibitor, nelfinavir, into cerebrospinal fluid (CSF). METHODS Nelfinavir, a commonly used HIV-1 protease inhibitor (PI), is highly effective for reducing plasma viral load. It is deployed clinically in combination with other antiretroviral

Comparative neurovirulence in lentiviral infections: The roles of viral molecular diversity and select proteases.

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All lentiviruses infect the brain, causing chronic neurological disease in their respective hosts. To examine the relationship(s) between lentivirus molecular diversity and the development of neurological disease, we examined in vitro and in vivo models of lentivirus neurovirulence using different

Role of P-glycoprotein on the CNS disposition of amprenavir (141W94), an HIV protease inhibitor.

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OBJECTIVE To determine the role of P-glycoprotein (Pgp) on the CNS penetration of the HIV protease inhibitor (PI) amprenavir (141W94) and to test the hypothesis that co-administration of a second HIV PI (ritonavir) could enhance amprenavir's brain penetration in vivo. METHODS Pgp-mediated efflux was

HIV-related neuropathology, 1985 to 1999: rising prevalence of HIV encephalopathy in the era of highly active antiretroviral therapy.

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Postmortem neuropathologic reports for a consecutive series of 436 HIV-seropositive patients who died between 1985 and 1999 were matched with clinical data for 371 of them. Cases were divided into four groups depending on the date of death. The chosen time periods reflected the type of

[A case of HIV encephalopathy with dementia which showed significant improvement after the combination antiretroviral therapy].

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We report a 63-year-old male with HIV encephalopathy, whose initial symptom was acutely progressing dementia. He tested positive for HIV antibody, and HIV-RNA count was 2.8 x 10(5) copy/ml. All opportunistic infections that could cause dementia were ruled out. Dementia remarkably improved after the

HIV protease inhibitor ritonavir: a more potent inhibitor of P-glycoprotein than the cyclosporine analog SDZ PSC 833.

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The effect of P-glycoprotein inhibition on the uptake of the HIV type 1 protease inhibitor saquinavir into brain capillary endothelial cells was studied using porcine primary brain capillary endothelial cell monolayers as an in vitro test system. As confirmed by polymerase chain reaction and Western

Molecular and cellular mechanisms of neuronal cell death in HIV dementia.

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The deaths of neurons, astrocytes and endothelial cells have been described in patients with HIV (human immunodeficiency virus) dementia. HIV-1 does not infect neurons; instead, neurotoxic substances shed by infected glia and macrophages can induce a form of programmed cell death called apoptosis in

HIV-1 gp120 upregulates matrix metalloproteinases and their inhibitors in a rat model of HIV encephalopathy.

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Matrix metalloproteinases (MMPs) are implicated in diverse processes, such as neuroinflammation, leakiness of the blood-brain barrier (BBB) and direct cellular damage in neurodegenerative and other CNS diseases. Tissue destruction by MMPs is regulated by their endogenous tissue inhibitors (TIMPs).

Beta amyloid levels in CSF of HIV-infected people vary by exposure to antiretroviral therapy.

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HIV-associated neurocognitive disorders (HAND) persist despite the widespread implementation of combined antiretroviral therapy (ART). As people with HIV (PWH) age on ART regimens, the risk of age-related comorbidities such as Alzheimer's disease (AD) may increase. However, questions

Anti-platelet-activating factor effects of highly active antiretroviral therapy (HAART): a new insight in the drug therapy of HIV infection?

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Platelet-activating factor (PAF) is a potent inflammatory mediator, which seems to play a role in the pathogenesis of several AIDS manifestations such as AIDS dementia complex, Kaposi's sarcoma, and HIV-related nephropathy. PAF antagonists have been studied in these conditions with promising

Activation of cyclin-dependent kinase 5 by calpains contributes to human immunodeficiency virus-induced neurotoxicity.

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Although the specific mechanism of neuronal damage in human immunodeficiency virus (HIV) -associated dementia is not known, a prominent role for NMDA receptor (NMDAR)-induced excitotoxicity has been demonstrated in neurons exposed to HIV-infected/activated macrophages. We hypothesized NMDAR-mediated

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