All Relations between Alzheimer Disease and microtubule-associated protein tau

Publication Sentence Publish Date Extraction Date Species
Jin Liu, Ding Wang, Shu-Qin Li, Yang Yu, Richard D Y. Suppression of LPS-induced tau hyperphosphorylation by serum amyloid A. Journal of neuroinflammation. vol 13. 2016-10-05. PMID:26838764. suppression of lps-induced tau hyperphosphorylation by serum amyloid a. accumulation of hyperphosphorylated tau is a major neuropathological feature of tauopathies including alzheimer's disease (ad). 2016-10-05 2023-08-13 Not clear
Kuo-Hsuan Chang, I-Cheng Chen, Hsuan-Yuan Lin, Hsuan-Chiang Chen, Chih-Hsin Lin, Te-Hsien Lin, Yu-Ting Weng, Chih-Ying Chao, Yih-Ru Wu, Jung-Yaw Lin, Guey-Jen Lee-Chen, Chiung-Mei Che. The aqueous extract of Glycyrrhiza inflata can upregulate unfolded protein response-mediated chaperones to reduce tau misfolding in cell models of Alzheimer's disease. Drug design, development and therapy. vol 10. 2016-10-05. PMID:27013866. the aqueous extract of glycyrrhiza inflata can upregulate unfolded protein response-mediated chaperones to reduce tau misfolding in cell models of alzheimer's disease. 2016-10-05 2023-08-13 Not clear
Kuo-Hsuan Chang, I-Cheng Chen, Hsuan-Yuan Lin, Hsuan-Chiang Chen, Chih-Hsin Lin, Te-Hsien Lin, Yu-Ting Weng, Chih-Ying Chao, Yih-Ru Wu, Jung-Yaw Lin, Guey-Jen Lee-Chen, Chiung-Mei Che. The aqueous extract of Glycyrrhiza inflata can upregulate unfolded protein response-mediated chaperones to reduce tau misfolding in cell models of Alzheimer's disease. Drug design, development and therapy. vol 10. 2016-10-05. PMID:27013866. alzheimer's disease (ad) and several neurodegenerative disorders known as tauopathies are characterized by misfolding and aggregation of tau protein. 2016-10-05 2023-08-13 Not clear
Philip Scheltens, Kaj Blennow, Monique M B Breteler, Bart de Strooper, Giovanni B Frisoni, Stephen Salloway, Wiesje Maria Van der Flie. Alzheimer's disease. Lancet (London, England). vol 388. issue 10043. 2016-09-30. PMID:26921134. alzheimer's disease, the most prevalent cause of dementia, is still defined by the combined presence of amyloid and tau, but researchers are gradually moving away from the simple assumption of linear causality as proposed in the original amyloid hypothesis. 2016-09-30 2023-08-13 Not clear
Jada Lewis, Dennis W Dickso. Propagation of tau pathology: hypotheses, discoveries, and yet unresolved questions from experimental and human brain studies. Acta neuropathologica. vol 131. issue 1. 2016-09-29. PMID:26576562. tau is a microtubule-associated protein and a key regulator of microtubule stabilization as well as the main component of neurofibrillary tangles-a principle neuropathological hallmark of alzheimer's disease (ad)-as well as pleomorphic neuronal and glial inclusions in neurodegenerative tauopathies. 2016-09-29 2023-08-13 human
Michael Niblock, Tibor Hortobágyi, Claire Troakes, Safa Al-Sarraj, Carl Spickett, Rebecca Jones, Christopher E Shaw, Jean-Marc Gall. Lack of association between TDP-43 pathology and tau mis-splicing in Alzheimer's disease. Neurobiology of aging. vol 37. 2016-09-26. PMID:26507309. lack of association between tdp-43 pathology and tau mis-splicing in alzheimer's disease. 2016-09-26 2023-08-13 Not clear
Michael Niblock, Tibor Hortobágyi, Claire Troakes, Safa Al-Sarraj, Carl Spickett, Rebecca Jones, Christopher E Shaw, Jean-Marc Gall. Lack of association between TDP-43 pathology and tau mis-splicing in Alzheimer's disease. Neurobiology of aging. vol 37. 2016-09-26. PMID:26507309. considering the pathogenic role of tau mis-splicing, we compared tau isoform expression between alzheimer's disease cases with or without tdp-43 inclusions. 2016-09-26 2023-08-13 Not clear
Michael Niblock, Tibor Hortobágyi, Claire Troakes, Safa Al-Sarraj, Carl Spickett, Rebecca Jones, Christopher E Shaw, Jean-Marc Gall. Lack of association between TDP-43 pathology and tau mis-splicing in Alzheimer's disease. Neurobiology of aging. vol 37. 2016-09-26. PMID:26507309. although tdp-43 functions may be affected, tdp-43 does not critically regulate expression or splicing of tau in alzheimer's disease suggesting that tdp-43 contributes to alzheimer's disease through mechanisms independent of tau. 2016-09-26 2023-08-13 Not clear
Orestes V Forlenza, Ivan Aprahamian, Márcia Radanovic, Leda L Talib, Marina Za Camargo, Florindo Stella, Rodrigo Machado-Vieira, Wagner F Gatta. Cognitive impairment in late-life bipolar disorder is not associated with Alzheimer's disease pathological signature in the cerebrospinal fluid. Bipolar disorders. vol 18. issue 1. 2016-09-26. PMID:26876913. it is uncertain whether cognitively impaired patients with bd may present the alzheimer's disease (ad) bio-signature in the cerebrospinal fluid (csf), defined as a combination of low concentrations of the amyloid-beta peptide (aβ1-42 ) and high concentrations of total tau (t-tau) and tau phosphorylated at threonine 181 (p-tau). 2016-09-26 2023-08-13 Not clear
Zhiyou Cai, Ming Xia. Oligodendrocytes and Alzheimer's disease. The International journal of neuroscience. vol 126. issue 2. 2016-09-21. PMID:26000818. extensive evidence has indicated that the breakdown of myelin is associated with alzheimer's disease (ad) since the vulnerability of oligodendrocytes under alzheimer's pathology easily induces the myelin breakdown and the loss of the myelin sheath which might be the initiating step in the changes of the earliest stage of ad prior to appearance of amyloid and tau pathology. 2016-09-21 2023-08-13 Not clear
Teemu Natunen, Mari Takalo, Susanna Kemppainen, Stina Leskelä, Mikael Marttinen, Kaisa M A Kurkinen, Juha-Pekka Pursiheimo, Timo Sarajärvi, Jayashree Viswanathan, Sami Gabbouj, Eino Solje, Eveliina Tahvanainen, Tiina Pirttimäki, Mitja Kurki, Jussi Paananen, Tuomas Rauramaa, Pasi Miettinen, Petra Mäkinen, Ville Leinonen, Hilkka Soininen, Kari Airenne, Rudolph E Tanzi, Heikki Tanila, Annakaisa Haapasalo, Mikko Hiltune. Relationship between ubiquilin-1 and BACE1 in human Alzheimer's disease and APdE9 transgenic mouse brain and cell-based models. Neurobiology of disease. vol 85. 2016-09-21. PMID:26563932. accumulation of β-amyloid (aβ) and phosphorylated tau in the brain are central events underlying alzheimer's disease (ad) pathogenesis. 2016-09-21 2023-08-13 mouse
Einar M Sigurdsso. Tau Immunotherapy. Neuro-degenerative diseases. vol 16. issue 1-2. 2016-09-20. PMID:26551002. phase i clinical trials on active and passive tau immunizations are being conducted, with several additional passive tau antibody trials likely to be initiated in the near future for alzheimer's disease and other tauopathies. 2016-09-20 2023-08-13 human
Ioannis Sotiropoulos, Nuno Sous. Tau as the Converging Protein between Chronic Stress and Alzheimer's Disease Synaptic Pathology. Neuro-degenerative diseases. vol 16. issue 1-2. 2016-09-20. PMID:26551025. tau as the converging protein between chronic stress and alzheimer's disease synaptic pathology. 2016-09-20 2023-08-13 Not clear
Alba Sierra-Rio, Mircea Balasa, Jaume Olives, Anna Antonell, Alex Iranzo, Magda Castellví, Beatriz Bosch, Oriol Grau-Rivera, Guadalupe Fernandez-Villullas, Lorena Rami, Albert Lladó, Raquel Sánchez-Valle, José Luis Molinuev. Cerebrospinal Fluid Biomarkers Predict Clinical Evolution in Patients with Subjective Cognitive Decline and Mild Cognitive Impairment. Neuro-degenerative diseases. vol 16. issue 1-2. 2016-09-20. PMID:26560503. determination of alzheimer's disease (ad) by cerebrospinal fluid (csf) biomarkers - 42-amino-acid amyloid-β (aβ42), total tau and phosphorylated tau (p-tau) - has demonstrated high validity for detecting ad neuropathological changes. 2016-09-20 2023-08-13 human
Jennifer M Deger, Julia E Gerson, Rakez Kaye. The interrelationship of proteasome impairment and oligomeric intermediates in neurodegeneration. Aging cell. vol 14. issue 5. 2016-09-19. PMID:26053162. many proteins involved in neurodegeneration have been found to be sumoylated, notably tau protein in brains afflicted with alzheimer's. 2016-09-19 2023-08-13 Not clear
Yan Wei, Chanshuai Han, Yujing Wang, Beibei Wu, Tao Su, Ying Liu, Rongqiao H. Ribosylation triggering Alzheimer's disease-like Tau hyperphosphorylation via activation of CaMKII. Aging cell. vol 14. issue 5. 2016-09-19. PMID:26095350. ribosylation triggering alzheimer's disease-like tau hyperphosphorylation via activation of camkii. 2016-09-19 2023-08-13 mouse
Yan Wei, Chanshuai Han, Yujing Wang, Beibei Wu, Tao Su, Ying Liu, Rongqiao H. Ribosylation triggering Alzheimer's disease-like Tau hyperphosphorylation via activation of CaMKII. Aging cell. vol 14. issue 5. 2016-09-19. PMID:26095350. targeting ribosylation by inhibiting age formation may be a promising therapeutic strategy to prevent alzheimer's disease-like tau hyperphosphorylation and diabetic encephalopathies. 2016-09-19 2023-08-13 mouse
Jonathan Spiegel, Elizabeth Pirraglia, Ricardo S Osorio, Lidia Glodzik, Yi Li, Wai Tsui, Leslie A Saint Louis, Catherine Randall, Tracy Butler, Jinfeng Xu, Raymond P Zinkowski, Henrik Zetterberg, Juan Fortea, Silvia Fossati, Thomas Wisniewski, Peter Davies, Kaj Blennow, Mony J de Leo. Greater specificity for cerebrospinal fluid P-tau231 over P-tau181 in the differentiation of healthy controls from Alzheimer's disease. Journal of Alzheimer's disease : JAD. vol 49. issue 1. 2016-09-19. PMID:26444757. cerebrospinal fluid (csf) measures of phosphorylated-tau (p-tau) 231 and p-tau181 are two biomarkers for the identification of tau pathology as related to alzheimer's disease (ad). 2016-09-19 2023-08-13 human
Laura B Eisenmenger, Eugene J Huo, John M Hoffman, Satoshi Minoshima, Manuela C Matesan, David H Lewis, Brian J Lopresti, Chester A Mathis, David O Okonkwo, James M Mount. Advances in PET Imaging of Degenerative, Cerebrovascular, and Traumatic Causes of Dementia. Seminars in nuclear medicine. vol 46. issue 1. 2016-09-19. PMID:26687858. in addition, the recognition of the importance of neocortical neurofibrillary tangles as related to alzheimer disease progression has led to the development of promising tau imaging agents such as [(18)f]t807. 2016-09-19 2023-08-13 Not clear
C Laurent, S Burnouf, B Ferry, V L Batalha, J E Coelho, Y Baqi, E Malik, E Mariciniak, S Parrot, A Van der Jeugd, E Faivre, V Flaten, C Ledent, R D'Hooge, N Sergeant, M Hamdane, S Humez, C E Müller, L V Lopes, L Buée, D Blu. A2A adenosine receptor deletion is protective in a mouse model of Tauopathy. Molecular psychiatry. vol 21. issue 1. 2016-09-16. PMID:25450226. consumption of caffeine, a non-selective adenosine a2a receptor (a2ar) antagonist, reduces the risk of developing alzheimer's disease (ad) in humans and mitigates both amyloid and tau burden in transgenic mouse models. 2016-09-16 2023-08-13 mouse