| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Hanno M Rode. Prospect of therapeutic approaches to tauopathies. Journal of molecular neuroscience : MN. vol 20. issue 2. 2003-08-18. PMID:12794313. |
aggregated tau in all tauopathies including ad is abnormally modified by the excess incorporation of chemical groups called phosphates (hyperphosphorylation), and the appearance of this biochemical change coincides with the onset all tauopathies, suggesting that it is both a necessary and sufficient cause for such diseases. |
2003-08-18 |
2023-08-12 |
Not clear |
| Kelly L Krass, Veronica Colinayo, Anatole Ghazalpour, Harry V Vinters, Aldons J Lusis, Thomas A Drak. Genetic loci contributing to age-related hippocampal lesions in mice. Neurobiology of disease. vol 13. issue 2. 2003-08-08. PMID:12828934. |
c57bl/6j mice develop genetically determined age-related hippocampal granular deposits that have some similarities to lesions seen in the brains of human patients with tau protein related neurodegenerative disorders ("tauopathies"). |
2003-08-08 |
2023-08-12 |
mouse |
| R de Silva, T Lashley, G Gibb, D Hanger, A Hope, A Reid, R Bandopadhyay, M Utton, C Strand, T Jowett, N Khan, B Anderton, N Wood, J Holton, T Revesz, A Lee. Pathological inclusion bodies in tauopathies contain distinct complements of tau with three or four microtubule-binding repeat domains as demonstrated by new specific monoclonal antibodies. Neuropathology and applied neurobiology. vol 29. issue 3. 2003-07-31. PMID:12787326. |
pathological inclusion bodies in tauopathies contain distinct complements of tau with three or four microtubule-binding repeat domains as demonstrated by new specific monoclonal antibodies. |
2003-07-31 |
2023-08-12 |
human |
| R de Silva, T Lashley, G Gibb, D Hanger, A Hope, A Reid, R Bandopadhyay, M Utton, C Strand, T Jowett, N Khan, B Anderton, N Wood, J Holton, T Revesz, A Lee. Pathological inclusion bodies in tauopathies contain distinct complements of tau with three or four microtubule-binding repeat domains as demonstrated by new specific monoclonal antibodies. Neuropathology and applied neurobiology. vol 29. issue 3. 2003-07-31. PMID:12787326. |
pathological inclusions containing fibrillar aggregates of hyperphosphorylated tau protein are a characteristic feature in the tauopathies, which include alzheimer's disease, frontotemporal dementia with parkinsonism linked to chromosome 17 (ftdp-17), progressive supranuclear palsy, corticobasal degeneration and pick's disease. |
2003-07-31 |
2023-08-12 |
human |
| R de Silva, T Lashley, G Gibb, D Hanger, A Hope, A Reid, R Bandopadhyay, M Utton, C Strand, T Jowett, N Khan, B Anderton, N Wood, J Holton, T Revesz, A Lee. Pathological inclusion bodies in tauopathies contain distinct complements of tau with three or four microtubule-binding repeat domains as demonstrated by new specific monoclonal antibodies. Neuropathology and applied neurobiology. vol 29. issue 3. 2003-07-31. PMID:12787326. |
we have investigated changes in the ratio and distribution of three-repeat and four-repeat tau in the different tauopathies as a basis of the phenotypic range of these disorders and the selective vulnerability of different subsets of neurones. |
2003-07-31 |
2023-08-12 |
human |
| Zhihong Jiang, Hao Tang, Necat Havlioglu, Xiaochun Zhang, Stefan Stamm, Riqiang Yan, Jane Y W. Mutations in tau gene exon 10 associated with FTDP-17 alter the activity of an exonic splicing enhancer to interact with Tra2 beta. The Journal of biological chemistry. vol 278. issue 21. 2003-07-07. PMID:12649279. |
our results implicate the human tau gene as a target gene for the alternative splicing regulator tra2 beta, suggesting that tra2 beta may play a role in aberrant tau exon 10 alternative splicing and in the pathogenesis of tauopathies. |
2003-07-07 |
2023-08-12 |
human |
| Victoria Zhukareva, Sonali Sundarraj, David Mann, Magnus Sjogren, Kaj Blenow, Christopher M Clark, Daniel W McKeel, Alison Goate, Carol F Lippa, Jean-Paul Vonsattel, John H Growdon, John Q Trojanowski, Virginia M-Y Le. Selective reduction of soluble tau proteins in sporadic and familial frontotemporal dementias: an international follow-up study. Acta neuropathologica. vol 105. issue 5. 2003-06-06. PMID:12677447. |
these findings confirm and extend the definition of dldh as a sporadic or familial "tau-less" tauopathy with reduced levels of soluble brain tau and no insoluble tau or fibrillary tau inclusions, and the data also underline the phenotypic heterogeneity of hddd2, which parallels the phenotypic heterogeneity of other hereditary neurodegenerative ftd tauopathies caused by tau gene mutations. |
2003-06-06 |
2023-08-12 |
Not clear |
| Yoshio Tsuboi, Zbigniew K Wszolek, Yoshikuni Mizuno, Tomonori Kobayashi, Minoru Yasuda, Tatsuo Yamad. [Japanese contribution to the understanding of frontotemporal dementia and parkinsonism linked to chromosome 17(FTDP-17)]. No to shinkei = Brain and nerve. vol 55. issue 2. 2003-06-06. PMID:12684990. |
autopsies demonstrate the presence of neuronal and glial tau inclusions and ballooned neurons, frequently in the distribution seen in other sporadic tauopathies. |
2003-06-06 |
2023-08-12 |
Not clear |
| Alberto Gómez-Ramos, Javier Díaz-Nido, Mark A Smith, George Perry, Jesús Avil. Effect of the lipid peroxidation product acrolein on tau phosphorylation in neural cells. Journal of neuroscience research. vol 71. issue 6. 2003-05-07. PMID:12605413. |
a hallmark of several neurodegenerative disorders, including alzheimer's disease and tauopathies, is the hyperphosphorylation of the microtubule-associated protein tau. |
2003-05-07 |
2023-08-12 |
mouse |
| Alberto Gómez-Ramos, Javier Díaz-Nido, Mark A Smith, George Perry, Jesús Avil. Effect of the lipid peroxidation product acrolein on tau phosphorylation in neural cells. Journal of neuroscience research. vol 71. issue 6. 2003-05-07. PMID:12605413. |
these results support the view that oxidative stress and subsequent formation of lipid peroxidation products may contribute to tau protein phosphorylation in alzheimer's disease and tauopathies. |
2003-05-07 |
2023-08-12 |
mouse |
| Gail V W Johnson, Craig D C Baile. Tau, where are we now? Journal of Alzheimer's disease : JAD. vol 4. issue 5. 2003-04-04. PMID:12446970. |
further there is an ever growing family of neurodegenerative diseases called "tauopathies" where tau pathology is the primary, defining characteristic with little or no abeta pathology. |
2003-04-04 |
2023-08-12 |
Not clear |
| Gail V W Johnson, Craig D C Baile. Tau, where are we now? Journal of Alzheimer's disease : JAD. vol 4. issue 5. 2003-04-04. PMID:12446970. |
this review highlights recent findings concerning the normal metabolism and function of tau, as well as the abnormal processing and function of tau in alzheimer's disease and in the tauopathies, both sporadic and familial. |
2003-04-04 |
2023-08-12 |
Not clear |
| Javier Díaz-Nido, Francisco Wandosell, Jesús Avil. Glycosaminoglycans and beta-amyloid, prion and tau peptides in neurodegenerative diseases. Peptides. vol 23. issue 7. 2003-04-03. PMID:12128089. |
thus, beta-amyloid peptide (abeta) accumulates within senile amyloid plaques in ad, protease-resistant prion protein constitutes the amyloid deposits in spongiform encephalopathies and tau protein gives rise to neurofibrillary tangles (nft) both in ad and in tauopathies. |
2003-04-03 |
2023-08-12 |
Not clear |
| I Ferrer, M Barrachina, B Pui. Glycogen synthase kinase-3 is associated with neuronal and glial hyperphosphorylated tau deposits in Alzheimer's disease, Pick's disease, progressive supranuclear palsy and corticobasal degeneration. Acta neuropathologica. vol 104. issue 6. 2003-02-12. PMID:12410379. |
specific bands differing from those of phospho-tau were seen on western blots of sarcosyl-insoluble fractions processed for gsk-3alpha/beta and gsk-3beta-p. double-labeling immunohistochemistry discloses that gsk-3beta-p co-localizes with abnormal tau in about 50% of neurons with neurofibrillary tangles, and in neuronal processes, astrocytes and oligodendrocytes in various tauopathies. |
2003-02-12 |
2023-08-12 |
Not clear |
| I Ferrer, M Barrachina, B Pui. Glycogen synthase kinase-3 is associated with neuronal and glial hyperphosphorylated tau deposits in Alzheimer's disease, Pick's disease, progressive supranuclear palsy and corticobasal degeneration. Acta neuropathologica. vol 104. issue 6. 2003-02-12. PMID:12410379. |
moreover, the elevated number of tau-containing cells stained with anti-gsk-3beta-p antibodies suggests a partial inactivation of the kinase, or sequestration of the phosphorylated form, which may contribute to the regulation of the cascade of tau hyperphosphorylation in tauopathies, and to protect tau-containing cells from apoptosis. |
2003-02-12 |
2023-08-12 |
Not clear |
| I Ferrer, M Barrachina, B Pui. Anti-tau phospho-specific Ser262 antibody recognizes a variety of abnormal hyper-phosphorylated tau deposits in tauopathies including Pick bodies and argyrophilic grains. Acta neuropathologica. vol 104. issue 6. 2003-02-12. PMID:12410387. |
anti-tau phospho-specific ser262 antibody recognizes a variety of abnormal hyper-phosphorylated tau deposits in tauopathies including pick bodies and argyrophilic grains. |
2003-02-12 |
2023-08-12 |
rabbit |
| I Ferrer, M Barrachina, B Pui. Anti-tau phospho-specific Ser262 antibody recognizes a variety of abnormal hyper-phosphorylated tau deposits in tauopathies including Pick bodies and argyrophilic grains. Acta neuropathologica. vol 104. issue 6. 2003-02-12. PMID:12410387. |
this indicates postmortem modifications of tau in pick bodies and argyrophilic grains, but not in other tau-containing inclusions, including paired helical filaments and coiled bodies, and suggests differences in tau conformation, particularly that involving phospho-tau ser262 among tauopathies. |
2003-02-12 |
2023-08-12 |
rabbit |
| Garth F Hall, Sangmook Lee, Jun Ya. Neurofibrillary degeneration can be arrested in an in vivo cellular model of human tauopathy by application of a compound which inhibits tau filament formation in vitro. Journal of molecular neuroscience : MN. vol 19. issue 3. 2003-02-06. PMID:12540050. |
although tau filament formation is a central event in familial tauopathies and alzheimer's disease (ad), the cellular consequences of neurofibrillary tangle (nft) formation are poorly understood because of the unavailability of mammalian in vivo cellular models of neurofibrillary degeneration (nfd). |
2003-02-06 |
2023-08-12 |
human |
| Khalid Iqbal, Alejandra del C Alonso, Ezzat El-Akkad, Cheng-Xin Gong, Niloufar Haque, Sabiha Khatoon, Jin-Jing Pei, Ichiro Tsujio, Jian-Zhi Wang, Inge Grundke-Iqba. Significance and mechanism of Alzheimer neurofibrillary degeneration and therapeutic targets to inhibit this lesion. Journal of molecular neuroscience : MN. vol 19. issue 1-2. 2003-01-28. PMID:12212801. |
abnormally hyperphosphorylated tau which is the major protein subunit of paired helical filaments (phf)/neurofibrillary tangles is the pivotal lesion in alzheimer disease (ad) and related tauopathies. |
2003-01-28 |
2023-08-12 |
Not clear |
| Markus Tolnay, Alphonse Probs. Frontotemporal lobar degeneration--tau as a pied piper? Neurogenetics. vol 4. issue 2. 2003-01-23. PMID:12481984. |
the recent discovery of tau gene mutations in ftdp-17 brought tau to the center stage, but led to the erroneous trend of collectively grouping all forms of ftld as tauopathies. |
2003-01-23 |
2023-08-12 |
Not clear |