gliosis/protease

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HIV protease inhibitors disrupt astrocytic glutamate transporter function and neurobehavioral performance.

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OBJECTIVE The neurotoxic actions of the HIV protease inhibitors, amprenavir (APV) and lopinavir (LPV) were investigated. METHODS With combination antiretroviral therapy (cART), HIV-infected persons exhibit neurocognitive impairments, raising the possibility that cART might exert adverse central

Dissection and cotransplantation of large pieces of RPE and neural retina; effect of protease K on the development.

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OBJECTIVE This study attempts to cotransplant large pieces of the RPE and neural retina in the subretinal space of rabbits by using protease K for dissection of the donor tissue, and to investigate the effect of dissection technique on the development of the grafts. METHODS Eyes from 15-day-old

Familial progressive subcortical gliosis: presence of prions and linkage to chromosome 17.

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Progressive subcortical gliosis (PSG) is a sporadic and familial dementing disease characterized pathologically by astrogliosis at the cortex-white matter junction, a feature present in some prion diseases. With immunocytochemical and Western blot analyses, we investigated the presence of deposits

Dying neural cells activate glia through the release of a protease product.

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The close relationship between neurodegeneration and gliosis could play a relevant role in propagating the degenerative event in the brain. Although there is evidence of the neurotoxicity of activated glia, the ability of damaged neurons to modulate glial response remains unexplored. Exposure of

Protease inhibitor coinfusion with amyloid beta-protein results in enhanced deposition and toxicity in rat brain.

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Amyloid beta-protein, Abeta, is normally produced in brain and is cleared by unknown mechanisms. In Alzheimer's disease (AD), Abeta accumulates in plaque-like deposits and is implicated genetically in neurodegeneration. Here we investigate mechanisms for Abeta degradation and Abeta toxicity in vivo,

Calcium influx and activation of calpain I mediate acute reactive gliosis in injured spinal cord.

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Buffering extracellular pH at the site of a spinal cord crush-injury may stimulate axonal regeneration in rats (1; Guth et al., Exp. Neurol. 88: 44-55, 1985). We demonstrated in cultured astrocytes that acidic pH initiates a rapid increase in immunoreactivity for GFAP (GFAP-IR), a hallmark of

Absence of protease-resistant prion protein in dementia characterized by neuronal loss and status spongiosus.

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Dementia characterized by neuronal loss and status spongiosus (DNLS) is a non-Alzheimer degenerative process which is characterized by Pick-like lobar atrophy with neuronal depletion and gliosis of the cerebral cortex, corpus striatum, medial thalamus, and substantia nigra and the absence of

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

Protease-resistant PrP and PrP oligomers in the brain in human prion diseases after intraventricular pentosan polysulfate infusion.

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Intraventricular infusion of pentosan polysulfate (PPS) as a treatment for various human prion diseases has been applied in Japan. To evaluate the influence of PPS treatment we performed pathological examination and biochemical analyses of PrP molecules in autopsied brains treated with PPS (one case

Motor neuron cell death in wobbler mutant mice follows overexpression of the G-protein-coupled, protease-activated receptor for thrombin.

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BACKGROUND Mechanisms underlying neurodegeneration are actively sought for new therapeutic strategies. Transgenic, knockout and genetic mouse models greatly aid our understanding of the mechanisms for neuronal cell death. A naturally occurring, autosomal recessive mutant, known as wobbler, and mice

Early cytokine elevation, PrPres deposition, and gliosis in mouse scrapie: no effect on disease by deletion of cytokine genes IL-12p40 and IL-12p35.

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Neurodegenerative diseases are typically associated with an activation of glia and an increased level of cytokines. In our previous studies of prion disease, the cytokine response in the brains of clinically sick scrapie-infected mice was restricted to a small group of cytokines, of which IL-12p40,

A novel form of human disease with a protease-sensitive prion protein and heterozygosity methionine/valine at codon 129: Case report.

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BACKGROUND Sporadic Creutzfeldt-Jakob disease (sCJD) is a rare neurodegenerative disorder in humans included in the group of Transmissible Spongiform Encephalopathies or prion diseases. The vast majority of sCJD cases are molecularly classified according to the abnormal prion protein (PrPSc)

Exacerbation of dopaminergic terminal damage in a mouse model of Parkinson's disease by the G-protein-coupled receptor protease-activated receptor 1.

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Protease-activated receptor 1 (PAR1) is a G-protein-coupled receptor activated by serine proteases and expressed in astrocytes, microglia, and specific neuronal populations. We examined the effects of genetic deletion and pharmacologic blockade of PAR1 in the mouse

Inhibition of reactive gliosis attenuates excitotoxicity-mediated death of retinal ganglion cells.

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Reactive gliosis is a hallmark of many retinal neurodegenerative conditions, including glaucoma. Although a majority of studies to date have concentrated on reactive gliosis in the optic nerve head, very few studies have been initiated to investigate the role of reactive gliosis in the retina. We

MAPK signal transduction underlying brain inflammation and gliosis as therapeutic target.

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A majority, if not all, acute and progressive neurodegenerative diseases are accompanied by local microglia-mediated inflammation, astrogliosis, infiltration of immune cells, and activation of the adaptive immunity. These processes progress by the expression of cytokines, adhesion molecules,

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