dementia/protease

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[The significance of measurement of contents of serum serine protease inhibitors in senile dementia of the Alzheimer type].

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We have evaluated serum alpha 1-antichymotrypsin content in dementia of the Alzheimer type (DAT). The subjects consisted of 26 patients with DAT, 15 with cerebrovascular dementia, 10 with mixed type dementia, 2 with Down syndrome, 17 with Parkinson disease, 14 with spinocerebellar degeneration, 14

Comparison of cathepsin protease activities in brain tissue from normal cases and cases with Alzheimer's disease, Lewy body dementia, Parkinson's disease and Huntington's disease.

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Recent evidence, based upon immunocytochemical and histochemical analysis of brain cortical tissue from alzheimer's disease patients, has suggested that altered activity and/or distribution of the lysosomal proteases cathepsins B and D may be implicated in the abnormal protein processing pathway

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

Upregulation of amyloid precursor protein isoforms containing Kunitz protease inhibitor in dementia with Lewy bodies.

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Amyloid precursor protein (APP) is involved in the accumulation of alpha-synuclein, the main component of Lewy bodies. It is currently unknown, however, whether any of the APP isoforms is instrumental in alpha-synuclein deposition in dementia with Lewy bodies (DLB). Using real-time RT-PCR, we have

Exploitation of HIV protease inhibitor Indinavir as a memory restorative agent in experimental dementia.

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The present study was undertaken to investigate the beneficial effect of HIV protease inhibitor Indinavir on memory deficits associated with experimental dementia of Alzheimer disease's (AD) type. Dementia was induced in Swiss albino mice by administration of Celecoxib (100 mg kg(-1) orally, daily

Variably protease-sensitive prionopathy mimicking frontotemporal dementia.

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Sporadic prion diseases are fatal neurodegenerative disorders characterized clinically by rapidly progressive dementia and myoclonus. Variably protease-sensitive prionopathy (VPSPr) is a recently identified sporadic human prion disorder that may present with a lengthy atypical clinical history.

Variably protease-sensitive prionopathy: A differential diagnostic consideration for dementia.

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Prion diseases are rare neurodegenerative diseases that are caused by abnormal pathogenic agents and can affect both humans and animals. These diseases are categorized as sporadic, inherited, or acquired by infection. Clinical manifestations include psychiatric symptoms, cognitive

Amyloid-beta deposition in the cerebral cortex in Dementia with Lewy bodies is accompanied by a relative increase in AbetaPP mRNA isoforms containing the Kunitz protease inhibitor.

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Deposition of amyloid-beta, the fibrillogenic product of the cell surface protein AbetaPP (amyloid-beta protein precursor), occurs in the cerebral cortex of patients with Dementia with Lewy bodies (DLB). Amyloid deposition, basically in the form of senile plaques, occurs not only in the common form

Protease inhibitors may reverse AIDS dementia.

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Clinical course and CSF amyloid beta protein precursor having the site of application of the protease inhibitor (APPI) levels in patients with dementia of the Alzheimer type.

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Will posttranslational modifications of brain proteins provide novel serological markers for dementias?

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Drug development for dementias is significantly hampered by the lack of easily accessible biomarkers. Fluid biomarkers of dementias provide indications of disease stage, but have little prognostic value, cannot detect early pathological changes, and can only be measured in CSF (cerebrospinal fluid)

High expression on Kunitz-type protease inhibitor-containing substances in the cerebral vessels of patients with Down syndrome.

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Down syndrome (DS) brains, from 19 gestational weeks to 50 years of age were studied by immunohistochemical methods with a polyclonal antibody against synthetic peptide comprising part of the Kunitz-type protease inhibitor (KPI) domain of Alzheimer disease amyloid precursor protein (APP), residues

Excessive urokinase-type plasminogen activator activity in the euglobulin fraction of patients with Alzheimer-type dementia.

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We examined the activity of the serine protease urokinase-type plasminogen activator (uPA) present in the euglobulin fraction of plasma from 17 demented patients with probable Alzheimer's disease (AD), 12 patients with vascular dementia (VD) and 10 healthy controls. Euglobulin protein fractions were

De novo seven extra repeat expanded mutation in the PRNP gene in an Italian patient with early onset dementia.

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Point and octapeptide repeat (24 bp) insertional mutations in the prion protein gene (PRNP) cause a dominantly transmitted dementia, associated with spongiform degeneration of the brain, astrocytic gliosis and neuronal loss due to cell accumulation of mutated protease resistant prion protein. The

The effects of Alzheimer's disease, other dementias, and premortem course on beta-amyloid precursor protein messenger RNA in frontal cortex.

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There are conflicting data regarding alterations in beta-amyloid precursor protein (APP) mRNAs in Alzheimer's disease (AD). This may be due partly to variables such as agonal state and choice of control group. We have used in situ hybridization histochemistry to study expression of APP mRNAs, with

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