Disease relevance of Supranuclear Palsy, Progressive

• Pathologic alterations in the microtubule-associated protein tau have been implicated in a number of neurodegenerative disorders, including Alzheimer's disease (AD), progressive supranuclear palsy (PSP), and frontotemporal dementia (FTD) [1].
• Ubiquitin was present not only in paired helical filaments that form the neurofibrillary tangle of Alzheimer disease, but also in the filamentous components of the inclusion characteristic of Parkinson disease, Pick disease, and progressive supranuclear palsy [2].
• PET imaging with [(18)F]-fluorodeoxyglucose (FDG) has been used to identify characteristic patterns of regional glucose metabolism in patient cohorts with idiopathic Parkinson's disease (PD), as well as variant forms of parkinsonism such as multiple system atrophy (MSA), progressive supranuclear palsy (PSP), and corticobasal degeneration (CBGD) [3].
• Dystonia in Parkinson's disease, multiple system atrophy, and progressive supranuclear palsy [4].
• This included three of seven Alzheimer disease, two of three Huntington disease, two of two Parkinson disease, one of one progressive supranuclear palsy, one of one acoustic neuroma, one of two cerebrovascular disease, and one of two Guamanian amyotrophic lateral sclerosis (ALS) [5].

Psychiatry related information on Supranuclear Palsy, Progressive

• Can tropicamide eye drop response differentiate patients with progressive supranuclear palsy and Alzheimer's disease from healthy control subjects [6]?
• Dementias characterized at onset by prominent motor signs include dementias with Lewy bodies, idiopathic Parkinson's disease, progressive supranuclear palsy, cortico-basal ganglionic degeneration, hydrocephalus, Huntington's disease, and vascular dementia [7].
• The visually evoked P 300 wave and related reaction times (RTs) were studied in 25 patients with progressive supranuclear palsy (PSP) [8].
• "Apraxia of eyelid opening" induced by levodopa therapy and apomorphine in atypical parkinsonism (possible progressive supranuclear palsy): a case report [9].

High impact information on Supranuclear Palsy, Progressive

• Neurofibrillary tangles (NFT) composed of the microtubule-associated protein tau are prominent in Alzheimer disease (AD), Pick disease, progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) [10].
• Zolpidem in progressive supranuclear palsy [11].
• Progressive supranuclear palsy: loss of striatal dopamine receptors demonstrated in vivo by positron tomography [12].
• None of the present cases was associated with progressive supranuclear palsy or with alpha-synuclein pathology [13].
• Phosphorylated map kinase (ERK1, ERK2) expression is associated with early tau deposition in neurones and glial cells, but not with increased nuclear DNA vulnerability and cell death, in Alzheimer disease, Pick's disease, progressive supranuclear palsy and corticobasal degeneration [14].

Chemical compound and disease context of Supranuclear Palsy, Progressive

• Levels of reduced glutathione are decreased in nigra in Parkinson's disease; this decrease does not occur in other brain areas or in other neurodegenerative illnesses affecting this brain region (i.e., multiple system atrophy, progressive supranuclear palsy) [15].
• PET measures of benzodiazepine receptors in progressive supranuclear palsy [16].
• Randomized placebo-controlled trial of donepezil in patients with progressive supranuclear palsy [17].
• Pramipexole in progressive supranuclear palsy [18].
• To confirm the preliminary report that increases in norepinephrine neurotransmission improve motor performance, we administered the investigational drug idazoxan (IDA) to nine patients with progressive supranuclear palsy (PSP) according to a double-blind crossover protocol [19].

Biological context of Supranuclear Palsy, Progressive

• Apolipoprotein E epsilon 4 allele frequency is not increased in progressive supranuclear palsy [20].
• We studied two candidate genes, tau (tau) and alpha-synuclein (SNCA), for evidence of linkage disequilibrium on a group of unrelated individuals with progressive supranuclear palsy (PSP) and a group of age-matched control subjects [21].
• Expression of the short transglutaminase 2 mRNA splice variant was not detectable in HD, although previous studies demonstrated upregulation in Alzheimer disease and progressive supranuclear palsy [22].
• BACKGROUND: Recent studies have shown an association between an extended tau haplotype (H1) that covers the entire human tau gene and progressive supranuclear palsy or, more inconsistently, other neurodegenerative disorders, such as corticobasal degeneration, Parkinson disease, Alzheimer disease, and frontotemporal dementia (FTD) [23].
• Receptor autoradiography with [3H]citalopram as ligand was used to study the distribution of serotonin uptake binding sites in post mortem brain tissues from patients with Parkinson's disease, progressive supranuclear palsy and from age-matched controls [24].

Anatomical context of Supranuclear Palsy, Progressive

• As the integrity of the omnipause neurons located in the nucleus raphe interpositus is a prerequisite of normal ocular motility, cell and neurofibrillary tangle densities were determined in 13 Steele-Richardson-Olszewski syndrome (SROS) cases [eight with supranuclear gaze palsy (SGP) and five without] and six controls [25].
• We performed a quantitative immunocytochemical study using a polyclonal antibody directed against choline acetyltransferase (ChAT) in the lower pontine reticular formation in four control subjects and three patients with progressive supranuclear palsy (PSP) [26].
• Using an antibody against choline acetyltransferase (ChAT), mesencephalic cholinergic cell nuclei were studied in autopsy material from 3 cases of progressive supranuclear palsy (PSP) and 4 controls [27].
• In order to evaluate the quantitative changes in the neostriatum in progressive supranuclear palsy (PSP), sections of the caudate head (CN) and putamen (PT) from 4 PSP patients were stained with Klüver-Barrera, and the cell body and nuclear area of the neurons were measured by a digitizer [28].
• Formic acid treatment exposes hidden neurofilament and tau epitopes in abnormal cytoskeletal filaments from patients with progressive supranuclear palsy and Alzheimer's disease [29].

Gene context of Supranuclear Palsy, Progressive

• MAPT, the gene encoding tau, was screened for mutations in 96 progressive supranuclear palsy subjects [30].
• Apolipoprotein E in progressive supranuclear palsy in Japan [31].
• Elevated levels of matrix metalloproteinases-9 and -1 and of tissue inhibitors of MMPs, TIMP-1 and TIMP-2 in postmortem brain tissue of progressive supranuclear palsy [32].
• Increase of cdk5 is related to neurofibrillary pathology in progressive supranuclear palsy [33].
• Multiple system atrophy/progressive supranuclear palsy: alpha-Synuclein, synphilin, tau, and APOE [34].

Analytical, diagnostic and therapeutic context of Supranuclear Palsy, Progressive

• Positron emission tomography study in progressive supranuclear palsy. Brain hypometabolic pattern and clinicometabolic correlations [35].
• Sequence analysis of tau 3'untranslated region and saitohin gene in sporadic progressive supranuclear palsy [36].
• Measurement of the dopaminergic degeneration in Parkinson's disease with [123I] beta-CIT and SPECT. Correlation with clinical findings and comparison with multiple system atrophy and progressive supranuclear palsy [37].
• Double-labeling immunohistochemistry to Bcl-2 and Bax and to tau protein was examined in the brains of patients with progressive supranuclear palsy (PSP) to study the possible relationship between the expression of Bax and Bcl-2 proteins and neurofibrillary tangle formation [38].
• Studies of crystallographic structure and composition of core nanocrystals of ferritin bound to aberrant tau filaments extracted from progressive supranuclear Palsy (PSP) and Alzheimer disease (AD) brain tissues were performed using high resolution transmission electron microscopy (HRTEM) and electron energy loss spectroscopy (EELS) [39].

References