Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P10636 (tau protein)
 5,110 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A novel brain-specific 25 kDa protein (p25) was purified from a bovine brain extract. The protein was phosphorylated by Ser/Thr-Pro kinase (TPK II) in tau protein kinase fractions at the Ser residues of Ser-Pro sequences. Using immunoblot analysis, the protein was found only in brain extracts, and was most abundant in the brain regions such as cerebrum and hippocampus, but less abundant in cerebellum, medulla oblongata and olfactory bulb. The protein was detected in rat, bovine and human brain extracts, indicating that this protein specifically exists in mammalian brain tissues.
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PMID:A novel brain-specific 25 kDa protein (p25) is phosphorylated by a Ser/Thr-Pro kinase (TPK II) from tau protein kinase fractions. 190 72

Newborn rat nasal tissues containing olfactory epithelium were dissociated and maintained in a monolayer cell culture. Neurons were present, as determined by immunostaining with antibodies to 4 neuron-specific proteins: neuron-specific enolase, microtubule-associated protein 2, tau protein and synaptophysin. Immunostained neurons had a distinctive morphology resembling olfactory neurons. By patch-clamp analysis, these cells were electrically active. Responses of some neurons to physiological concentrations of an odorant mixture identified them as olfactory receptor cells.
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PMID:Cultured rat olfactory neurons are excitable and respond to odors. 235 Aug 78

Main causes of dementia in the elderly are vascular dementia and Alzheimer's dementia. Vascular dementia is related to both amounts and localization of lesions. Recently incidence of diffuse vascular leukoencephalopathy (Binswanger type, leukoaraiosis) and amyloid angiopathy are increasing. In Alzheimer's protein chemistry of amyloid (beta protein, A4 protein) revealed its precursor APP and its gene (chromosome 21), which produces protease inhibitor in the brain of Alzheimer and Down's brains. APP is considered as an membrane protein (receptor) and appears abundantly in the cerebral cortex. Immunohistochemical study showed that beta protein is observed also in normal aged brain. On the other hand, tau protein (main component of Alzheimer's neurofibrillary tangle, PHF) appeared as abnormal sprouting of neurites in Alzheimer's brain. The latter may related to dementia and neural death. In Alzheimer's dementia, several neurotransmitters, including acetylcholine, are reduced in the brain and related structural changes are observed. Recently olfactory bulb and mucosal changes are remarked as one of pathogenesis of this disease. Delayed neuronal death is a new phenomenon of nerve cell death of vascular origin and should be studied in human vascular dementia.
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PMID:[Approach to the dementia research]. 269 99

Cell lines of continuously dividing human olfactory neuroblasts can be propagated using olfactory epithelium obtained from human donors at biopsy or autopsy. The expression of neuronal proteins in these cells, such as neurofilament protein and tau protein, can be increased using a combination of factors including nerve growth factor, fibroblast growth factor, interleukin 1 and interleukin 6. These cells also express aspects of human disease. Olfactory neuroblasts generated from donors with the common, sporadic forms of Alzheimer's disease, show elevated levels of the direct precursor to beta-amyloid, the amyloid precursor protein C-terminal derivative (CTD). When treated with the lysosomal inhibitor chloroquine, immunoblots of Alzheimer olfactory neuroblasts show seven-fold higher levels of CTDs than immunoblots from age-matched control neuroblasts. The disease related increases in CTDs can be reversed by treatment with agents that increase intracellular cyclic adenosine monophosphate (cAMP), such as dibutyryl-cyclic-AMP, theophylline, and isoproterenol.
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PMID:A.E. Bennett Research Award 1993. Olfactory neuroblasts from Alzheimer donors: studies on APP processing and cell regulation. 811 Sep 10

Abnormal tau protein expression was immunohistochemically examined in biopsied human olfactory mucosa. The olfactory mucosa of 25 patients with olfactory disturbances, whose structures were relatively preserved, was immunostained with a polyclonal antibody derived from neurofibrillary tangles from the brains of patients with Alzheimer's disease. Abnormal tau protein immunoreactivity was found in the olfactory vesicles, dendrites and perikarya of the olfactory receptor cells in the epithelium and olfactory nerve bundles in the lamina propria. This immunoreactivity in the olfactory nerve bundles was observed in patients in their teens to 80's, and the immunoreactivity of the olfactory vesicles and dendrites of the olfactory receptor cells was widely distributed in patients in their 30's to 70's. On the other hand, the immunoreactivity of the perikarya of the olfactory receptor cells was observed only in patients in their 50's and 60's. These results indicate that abnormal tau protein accumulation of perikarya is a pathological change and is related to aging of the olfactory neurons.
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PMID:[Abnormal tau protein expression in biopsied human olfactory mucosa]. 816 44

Characteristic changes appearing in the biopsied olfactory mucosa of Alzheimer's disease (AD) patients were investigated using immunohistochemical staining. Specimens were obtained from 6 patients who were clinically diagnosed with AD, 2 patients with cerebrovascular dementia and 5 age-matched patients with olfactory disturbance without dementia. In most AD cases, polyclonal tau protein immunoreactivity was seen in the dendrites, perikarya of the olfactory receptor cells in the olfactory epithelium and the olfactory nerve bundles in the lamina propria. In a few cases, tau protein immunoreactivity was found in the extracellular mass in the epithelium. Ubiquitin immunoreactivity was seen is the dendrites of olfactory receptor cells. On the other hand, in control cases, only dendrites and olfactory nerve bundles reacted to anti-polyclonal tau protein antiserum in a few cases. These results indicate that the neurofibrillary tangle-like tau protein immunoreactivity in the perikarya senile plaque-like extracellular mass and ubiquitin immunoreactivity in the olfactory epithelium were characteristic changes in AD, and olfactory mucosal biopsy is a useful method for the definitive diagnosis of AD.
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PMID:[Definitive diagnosis of Alzheimer's disease using olfactory mucosal biopsy]. 817 37

Characteristic changes that appear in the biopsied olfactory mucosa of patients with Alzheimer's disease (AD) were examined with immunohistochemical staining. Specimens were obtained from patients with clinical diagnoses of AD. Patients with vascular dementia and age-matched patients without dementia were used for controls. In most AD cases, neurofibrillary tangle-like abnormal tau protein (Tau) immunoreactivity was seen in the dendrites and perikarya of the olfactory receptor cells and in the nerve bundles. A senile plaque-like extracellular mass was found in the olfactory epithelium, and it reacted strongly to an anti-Tau antiserum and weakly to an anti-amyloid-beta protein antiserum. Ubiquitin (Ubq) immunoreactivity was also observed in the dendrites. Tau immunoreactivity of the perikarya and extracellular mass, and Ubq immunoreactivity were especially characteristic of the olfactory mucosa of AD patients. From these results, it is clear that the same pathologic changes in the brain are also present in the olfactory mucosa of patients with AD. Not only disruption of the central olfactory pathway, but also an olfactory disturbance of AD patients is caused by peripheral changes. Furthermore, an olfactory mucosal biopsy could be a useful method for a definitive diagnosis of AD.
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PMID:Pathology of olfactory mucosa in patients with Alzheimer's disease. 820 7

Neuropathological changes such as dystrophic neurites and the presence of abnormal tau protein in the olfactory system, including primary sensory cells and nerve fibres have previously been demonstrated in nasal mucosa tissue of patients with Alzheimer's disease (AD). These changes were detected in autopsy-derived material from histopathologically confirmed AD cases as well as in biopsy tissue from clinical severely ill AD patients. To investigate the potential usefulness for the early diagnosis of AD, we obtained biopsy tissue from olfactory mucosa from 5 clinically mild to moderate AD patients and stained for the presence of tau or beta-amyloid by immunocytochemistry using a panel of specific antibodies. No positive staining was found in any of the cases. For comparison, post-mortem olfactory tissue from AD patients with severe neuropathological changes (widespread neurofibrillary tangles and amyloid in the brain) was investigated. In these severe cases, tau immunoreactivity was found in fine nerve fibres in the lamina propria and in a few olfactory epithelial cells. These results are consistent with other reports showing that cytoskeletal changes and tau pathology in the olfactory epithelium are not primary (or specific) features of AD and may occur predominantly in late stages of the disease.
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PMID:Histological markers in nasal mucosa of patients with Alzheimer's disease. 969 30

JNPL3 transgenic mice expressing a mutant tau protein, which develop neurofibrillary tangles and progressive motor disturbance, were crossed with Tg2576 transgenic mice expressing mutant beta-amyloid precursor protein (APP), thus modulating the APP-Abeta (beta-amyloid peptide) environment. The resulting double mutant (tau/APP) progeny and the Tg2576 parental strain developed Abeta deposits at the same age; however, relative to JNPL3 mice, the double mutants exhibited neurofibrillary tangle pathology that was substantially enhanced in the limbic system and olfactory cortex. These results indicate that either APP or Abeta influences the formation of neurofibrillary tangles. The interaction between Abeta and tau pathologies in these mice supports the hypothesis that a similar interaction occurs in Alzheimer's disease.
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PMID:Enhanced neurofibrillary degeneration in transgenic mice expressing mutant tau and APP. 1152 Sep 74

Cumulative evidence suggests that neural network formation requires an ingenious regulation of the attractive and repulsive responses of growing axons to guidance cues. We examined the role of intracellular protein kinase A (PKA) signaling in the axonal pathfinding of olfactory sensory neurons in transparent zebrafish embryos. Microinjection of an olfactory marker protein gene promoter-driven double-cassette vector directed the expression of both the dominant form of PKA and green fluorescent protein fused with the microtubule-associated protein tau in the same olfactory neurons. The dominant-negative form of PKA enhanced the turning of olfactory neuron axons in the olfactory placode, whereas the disturbance effect of the constitutively active form on the axonal pathfinding was prominent in the olfactory bulb. Consistently, forskolin treatment severely inhibited the axonal extension in the olfactory bulb, but not in the olfactory placode. These results suggest that the switching of PKA signaling in developing olfactory sensory neurons is important for axonal pathfinding through the boundary between the olfactory placode and the olfactory bulb in vivo. We thus propose that the regulation of PKA signaling plays a key role in the long-distance axonal pathfinding through intermediate guideposts.
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PMID:Regulation by protein kinase A switching of axonal pathfinding of zebrafish olfactory sensory neurons through the olfactory placode-olfactory bulb boundary. 1207 93


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