All Relations between Alzheimer Disease and microtubule-associated protein tau

Publication Sentence Publish Date Extraction Date Species
Chiara D'Ambrosio, Simona Arena, Gabriella Fulcoli, Meir H Scheinfeld, Dawang Zhou, Luciano D'Adamio, Andrea Scalon. Hyperphosphorylation of JNK-interacting protein 1, a protein associated with Alzheimer disease. Molecular & cellular proteomics : MCP. vol 5. issue 1. 2006-03-28. PMID:16195223. this motif is modified by various kinases in aggregates of the microtubule-associated protein tau, which generates typical intraneuronal lesions occurring in alzheimer disease. 2006-03-28 2023-08-12 Not clear
Jian-Ping Guo, Tetsuaki Arai, Judit Miklossy, Patrick L McGee. Abeta and tau form soluble complexes that may promote self aggregation of both into the insoluble forms observed in Alzheimer's disease. Proceedings of the National Academy of Sciences of the United States of America. vol 103. issue 6. 2006-03-23. PMID:16446437. abeta and tau form soluble complexes that may promote self aggregation of both into the insoluble forms observed in alzheimer's disease. 2006-03-23 2023-08-12 Not clear
Brian Webster, Lawrence Hansen, Anthony Adame, Leslie Crews, Magdalena Torrance, Leon Thal, Eliezer Maslia. Astroglial activation of extracellular-regulated kinase in early stages of Alzheimer disease. Journal of neuropathology and experimental neurology. vol 65. issue 2. 2006-03-22. PMID:16462205. characterization of the earliest neuropathologic features of alzheimer disease (ad) indicates that synaptic degeneration accompanied by tau hyperphosphorylation and amyloid deposition might be an important feature. 2006-03-22 2023-08-12 Not clear
Salvatore Oddo, Antonella Caccamo, Levina Tran, Mary P Lambert, Charles G Glabe, William L Klein, Frank M LaFerl. Temporal profile of amyloid-beta (Abeta) oligomerization in an in vivo model of Alzheimer disease. A link between Abeta and tau pathology. The Journal of biological chemistry. vol 281. issue 3. 2006-03-17. PMID:16282321. accumulation of amyloid-beta (abeta) is one of the earliest molecular events in alzheimer disease (ad), whereas tau pathology is thought to be a later downstream event. 2006-03-17 2023-08-12 mouse
Deepa V Dabir, Michael B Robinson, Eric Swanson, Bin Zhang, John Q Trojanowski, Virginia M-Y Lee, Mark S Forma. Impaired glutamate transport in a mouse model of tau pathology in astrocytes. The Journal of neuroscience : the official journal of the Society for Neuroscience. vol 26. issue 2. 2006-03-17. PMID:16407562. less robust changes were observed in alzheimer's disease in which neuronal tau pathology predominates. 2006-03-17 2023-08-12 mouse
Khalid Iqbal, Michael Flory, Sabiha Khatoon, Hilkka Soininen, Tuula Pirttila, Maarit Lehtovirta, Irina Alafuzoff, Kaj Blennow, Niels Andreasen, Eugeen Vanmechelen, Inge Grundke-Iqba. Subgroups of Alzheimer's disease based on cerebrospinal fluid molecular markers. Annals of neurology. vol 58. issue 5. 2006-03-14. PMID:16247771. we immunoassayed levels of tau, ubiquitin, and abeta(1-42) in retrospectively collected csf samples of 468 clinically diagnosed alzheimer's disease patients (n = 353) or non-alzheimer's subjects (n = 115). 2006-03-14 2023-08-12 human
Khalid Iqbal, Michael Flory, Sabiha Khatoon, Hilkka Soininen, Tuula Pirttila, Maarit Lehtovirta, Irina Alafuzoff, Kaj Blennow, Niels Andreasen, Eugeen Vanmechelen, Inge Grundke-Iqba. Subgroups of Alzheimer's disease based on cerebrospinal fluid molecular markers. Annals of neurology. vol 58. issue 5. 2006-03-14. PMID:16247771. alzheimer's disease was subdivided into at least five subgroups based on csf levels of abeta(1-42), tau, and ubiquitin; each subgroup presented a different clinical profile. 2006-03-14 2023-08-12 human
Ricardo B Maccioni, Manuel Lavados, Marta Guillón, Cristina Mujica, Ruben Bosch, Gustavo Farías, Patricio Fuente. Anomalously phosphorylated tau and Abeta fragments in the CSF correlates with cognitive impairment in MCI subjects. Neurobiology of aging. vol 27. issue 2. 2006-03-14. PMID:16399209. alzheimer's disease (ad) is a neurodegenerative disorder characterized by the presence of extracellular amyloid deposits, consisting largely of abeta peptide and the presence of intraneuronal aggregates of neurofibillary tangles formed by tau. 2006-03-14 2023-08-12 human
Koji Tomoo, Tian-Ming Yao, Katsuhiko Minoura, Shuko Hiraoka, Miho Sumida, Taizo Taniguchi, Toshimasa Ishid. Possible role of each repeat structure of the microtubule-binding domain of the tau protein in in vitro aggregation. Journal of biochemistry. vol 138. issue 4. 2006-03-10. PMID:16272135. although one of the priorities in alzheimer's research is to clarify the filament formation mechanism of the tau protein, it is currently unclear how it is transformed from a normal structure in a neuron. 2006-03-10 2023-08-12 Not clear
Elena M Ribé, Mar Pérez, Berta Puig, Ignasi Gich, Filip Lim, Mar Cuadrado, Teresa Sesma, Silvia Catena, Belén Sánchez, María Nieto, Pilar Gómez-Ramos, M Asunción Morán, Felipe Cabodevilla, Lluis Samaranch, Lourdes Ortiz, Alberto Pérez, Isidro Ferrer, Jesús Avila, Teresa Gómez-Isl. Accelerated amyloid deposition, neurofibrillary degeneration and neuronal loss in double mutant APP/tau transgenic mice. Neurobiology of disease. vol 20. issue 3. 2006-03-09. PMID:16125396. even though the idea that amyloid beta peptide accumulation is the primary event in the pathogenesis of alzheimer's disease has become the leading hypothesis, the causal link between aberrant amyloid precursor protein processing and tau alterations in this type of dementia remains controversial. 2006-03-09 2023-08-12 mouse
Elena M Ribé, Mar Pérez, Berta Puig, Ignasi Gich, Filip Lim, Mar Cuadrado, Teresa Sesma, Silvia Catena, Belén Sánchez, María Nieto, Pilar Gómez-Ramos, M Asunción Morán, Felipe Cabodevilla, Lluis Samaranch, Lourdes Ortiz, Alberto Pérez, Isidro Ferrer, Jesús Avila, Teresa Gómez-Isl. Accelerated amyloid deposition, neurofibrillary degeneration and neuronal loss in double mutant APP/tau transgenic mice. Neurobiology of disease. vol 20. issue 3. 2006-03-09. PMID:16125396. these findings challenge the idea that tau pathology in alzheimer's disease is merely a downstream effect of amyloid production/deposition and suggest that reciprocal interactions between beta-amyloid and tau alterations may take place in vivo. 2006-03-09 2023-08-12 mouse
Lorella M T Canzoniero, B Joy Snide. Calcium in Alzheimer's disease pathogenesis: too much, too little or in the wrong place? Journal of Alzheimer's disease : JAD. vol 8. issue 2. 2006-03-08. PMID:16308483. the precise biophysical structure of the amyloid beta-peptide that causes neuronal dysfunction remains under investigation, as does the interaction between amyloid peptides and tau hyperphosphorylation, but these two molecules likely play key roles in neuronal dysfunction in alzheimer's disease. 2006-03-08 2023-08-12 Not clear
Randall L Woltjer, P J Cimino, Angela M Boutté, Aimee M Schantz, Kathleen S Montine, Eric B Larson, Thomas Bird, Joseph F Quinn, Jing Zhang, Thomas J Montin. Proteomic determination of widespread detergent-insolubility including Abeta but not tau early in the pathogenesis of Alzheimer's disease. FASEB journal : official publication of the Federation of American Societies for Experimental Biology. vol 19. issue 13. 2006-03-07. PMID:16129700. proteomic determination of widespread detergent-insolubility including abeta but not tau early in the pathogenesis of alzheimer's disease. 2006-03-07 2023-08-12 mouse
Nobuyuki Okamura, Takahiro Suemoto, Shozo Furumoto, Masako Suzuki, Hiroshi Shimadzu, Hiroyasu Akatsu, Takayuki Yamamoto, Hironori Fujiwara, Miyako Nemoto, Masahiro Maruyama, Hiroyuki Arai, Kazuhiko Yanai, Tohru Sawada, Yukitsuka Kud. Quinoline and benzimidazole derivatives: candidate probes for in vivo imaging of tau pathology in Alzheimer's disease. The Journal of neuroscience : the official journal of the Society for Neuroscience. vol 25. issue 47. 2006-03-07. PMID:16306398. quinoline and benzimidazole derivatives: candidate probes for in vivo imaging of tau pathology in alzheimer's disease. 2006-03-07 2023-08-12 mouse
Nobuyuki Okamura, Takahiro Suemoto, Shozo Furumoto, Masako Suzuki, Hiroshi Shimadzu, Hiroyasu Akatsu, Takayuki Yamamoto, Hironori Fujiwara, Miyako Nemoto, Masahiro Maruyama, Hiroyuki Arai, Kazuhiko Yanai, Tohru Sawada, Yukitsuka Kud. Quinoline and benzimidazole derivatives: candidate probes for in vivo imaging of tau pathology in Alzheimer's disease. The Journal of neuroscience : the official journal of the Society for Neuroscience. vol 25. issue 47. 2006-03-07. PMID:16306398. neurofibrillary tangles (nfts), neuropil threads, and neuritic elements of senile plaques predominantly comprise hyperphosphorylated tau protein and represent pathological characteristics of alzheimer's disease (ad). 2006-03-07 2023-08-12 mouse
Ing-Feng Chang, Huo-Yen Hsia. Induction of RhoGAP and pathological changes characteristic of Alzheimer's disease by UAHFEMF discharge in rat brain. Current Alzheimer research. vol 2. issue 5. 2006-03-07. PMID:16375659. novel experiments with ultrasound associated with high frequency electromagnetic field (uahfemf) irradiation on rats and mice found evidences of characteristic alzheimer's disease (ad) degenerations including neurite plaques, beta-amyloid, tau plaque and deposition in cells, neuro-fibrillary tangle and paired helical filament (phf) with rats and mice irradiated up to 2454 hours. 2006-03-07 2023-08-12 mouse
Cathy Andorfer, Christopher M Acker, Yvonne Kress, Patrick R Hof, Karen Duff, Peter Davie. Cell-cycle reentry and cell death in transgenic mice expressing nonmutant human tau isoforms. The Journal of neuroscience : the official journal of the Society for Neuroscience. vol 25. issue 22. 2006-03-02. PMID:15930395. mutations in the microtubule-associated protein tau gene have been linked to neurofibrillary tangle (nft) formation in several neurodegenerative diseases known as tauopathies; however, no tau mutations occur in alzheimer's disease, although this disease is also characterized by nft formation and cell death. 2006-03-02 2023-08-12 mouse
Jeffrey L Cumming. Treatment of Alzheimer's disease: current and future therapeutic approaches. Reviews in neurological diseases. vol 1. issue 2. 2006-03-02. PMID:16400259. the pathophysiology of alzheimer's disease (ad) includes the deposition of amyloid beta protein (abeta) and the ensuing initiation of a variety of secondary processes, including tau hyperphosphorylation, excitotoxicity, oxidation, and inflammation. 2006-03-02 2023-08-12 Not clear
Inna Khlistunova, Jacek Biernat, Yipeng Wang, Marcus Pickhardt, Martin von Bergen, Zuzana Gazova, Eckhard Mandelkow, Eva-Maria Mandelko. Inducible expression of Tau repeat domain in cell models of tauopathy: aggregation is toxic to cells but can be reversed by inhibitor drugs. The Journal of biological chemistry. vol 281. issue 2. 2006-02-28. PMID:16246844. the following three constructs were chosen: (i) the repeat domain of tau that coincides with the core of alzheimer paired helical filaments; (ii) the repeat domain with the deletion mutation deltak280 known from frontotemporal dementia and highly prone to spontaneous aggregation; and (iii) the repeat domain with deltak280 and two proline point mutations that inhibit aggregation. 2006-02-28 2023-08-12 Not clear
Shinichi Kosuga, Etsu Tashiro, Toshifumi Kajioka, Mayumi Ueki, Yoshifumi Shimizu, Masaya Imot. GSK-3beta directly phosphorylates and activates MARK2/PAR-1. The Journal of biological chemistry. vol 280. issue 52. 2006-02-27. PMID:16257959. in alzheimer disease (ad), the microtubule-associated protein tau is found hyperphosphorylated in paired helical filaments. 2006-02-27 2023-08-12 Not clear