All Relations between Alzheimer Disease and microtubule-associated protein tau

Publication Sentence Publish Date Extraction Date Species
Giulia M Sancesario, Sergio Bernardin. How many biomarkers to discriminate neurodegenerative dementia? Critical reviews in clinical laboratory sciences. vol 52. issue 6. 2016-08-02. PMID:26292074. opposite changes in the level of amyloid-β(1-42) versus total tau and phosphorylated-tau181 in the csf reflect the specific pathology of alzheimer's disease (ad) in the brain. 2016-08-02 2023-08-13 Not clear
Marie-Anne Burlot, Jérôme Braudeau, Kristin Michaelsen-Preusse, Brigitte Potier, Sophie Ayciriex, Jennifer Varin, Benoit Gautier, Fathia Djelti, Mickael Audrain, Luce Dauphinot, Francisco-Jose Fernandez-Gomez, Raphaëlle Caillierez, Olivier Laprévote, Ivan Bièche, Nicolas Auzeil, Marie-Claude Potier, Patrick Dutar, Martin Korte, Luc Buée, David Blum, Nathalie Cartie. Cholesterol 24-hydroxylase defect is implicated in memory impairments associated with Alzheimer-like Tau pathology. Human molecular genetics. vol 24. issue 21. 2016-08-02. PMID:26358780. alzheimer's disease (ad) is characterized by both amyloid and tau pathologies. 2016-08-02 2023-08-13 mouse
Caihong Zhu, Petra Schwarz, Irina Abakumova, Adriano Aguzz. Unaltered Prion Pathogenesis in a Mouse Model of High-Fat Diet-Induced Insulin Resistance. PloS one. vol 10. issue 12. 2016-08-01. PMID:26658276. in addition, impaired insulin signaling in the alzheimer's disease brain may promote aβ production, impair aβ clearance and induce tau hyperphosphorylation, thereby leading to deterioration of the disease. 2016-08-01 2023-08-13 mouse
Payam Emami Khoonsari, Anna Häggmark, Maria Lönnberg, Maria Mikus, Lena Kilander, Lars Lannfelt, Jonas Bergquist, Martin Ingelsson, Peter Nilsson, Kim Kultima, Ganna Shevchenk. Analysis of the Cerebrospinal Fluid Proteome in Alzheimer's Disease. PloS one. vol 11. issue 3. 2016-08-01. PMID:26950848. diagnosis of alzheimer's disease relies on cognitive tests and analysis of amyloid beta, protein tau, and hyperphosphorylated tau in cerebrospinal fluid. 2016-08-01 2023-08-13 Not clear
Diana L Castillo-Carranza, Marcos J Guerrero-Muñoz, Rakez Kaye. Immunotherapy for the treatment of Alzheimer's disease: amyloid-β or tau, which is the right target? ImmunoTargets and therapy. vol 3. 2016-07-29. PMID:27471697. immunotherapy for the treatment of alzheimer's disease: amyloid-β or tau, which is the right target? 2016-07-29 2023-08-13 mouse
Mark A MacLean, Elena Diez-Cecilia, Christopher B Lavery, Mark A Reed, Yanfei Wang, Donald F Weaver, Mark Stradiott. Diversification of edaravone via palladium-catalyzed hydrazine cross-coupling: Applications against protein misfolding and oligomerization of beta-amyloid. Bioorganic & medicinal chemistry letters. vol 26. issue 1. 2016-07-27. PMID:26598460. n-aryl derivatives of edaravone were identified as potentially effective small molecule inhibitors of tau and beta-amyloid aggregation in the context of developing disease-modifying therapeutics for alzheimer's disease (ad). 2016-07-27 2023-08-13 Not clear
James W Stevenson, Eliza A Conaty, Rylie B Walsh, Paul J Poidomani, Colin M Samoriski, Brianne J Scollins, Joseph A DeGiorgi. The Amyloid Precursor Protein of Alzheimer's Disease Clusters at the Organelle/Microtubule Interface on Organelles that Bind Microtubules in an ATP Dependent Manner. PloS one. vol 11. issue 1. 2016-07-26. PMID:26814888. although a direct kinesin/app association remains controversial, the distribution of app at the organelle/microtubule interface strongly suggests that app-organelles have an orientation and that app like the alzheimer's protein tau has a microtubule-based function. 2016-07-26 2023-08-13 human
Seyedeh Maryam Alavi Naini, Nadia Soussi-Yanicosta. Tau Hyperphosphorylation and Oxidative Stress, a Critical Vicious Circle in Neurodegenerative Tauopathies? Oxidative medicine and cellular longevity. vol 2015. 2016-07-25. PMID:26576216. hyperphosphorylation and aggregation of the microtubule-associated protein tau in brain, are pathological hallmarks of a large family of neurodegenerative disorders, named tauopathies, which include alzheimer's disease. 2016-07-25 2023-08-13 Not clear
Yukitsuka Kudo, Shozo Furumoto, Ryuichi Harada, Nobuyuki Okamur. [Tau imaging]. Nihon rinsho. Japanese journal of clinical medicine. vol 74. issue 3. 2016-07-25. PMID:27025077. in this paper we discussed some of the criteria required for the tau imaging probe in alzheimer's disease. 2016-07-25 2023-08-13 Not clear
Genjiro Suzuki, Masato Hasegaw. [The proceeding of drug development based on the propagation of tau protein]. Nihon rinsho. Japanese journal of clinical medicine. vol 74. issue 3. 2016-07-25. PMID:27025082. some neurodegenerative diseases such as alzheimer's disease are associated with the pathological aggregation of tau protein. 2016-07-25 2023-08-13 Not clear
Xuling Li, Peng Lei, Qingzhang Tuo, Scott Ayton, Qiao-Xin Li, Steve Moon, Irene Volitakis, Rong Liu, Colin L Masters, David I Finkelstein, Ashley I Bus. Enduring Elevations of Hippocampal Amyloid Precursor Protein and Iron Are Features of β-Amyloid Toxicity and Are Mediated by Tau. Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics. vol 12. issue 4. 2016-07-22. PMID:26260389. the amyloid cascade hypothesis of alzheimer's disease (ad) positions tau protein as a downstream mediator of β-amyloid (aβ) toxicity this is largely based on genetic cross breeding, which showed that tau ablation in young (3-7-month-old) transgenic mice overexpressing mutant amyloid precursor protein (app) abolished the phenotype of the app ad model. 2016-07-22 2023-08-13 mouse
Zhi-Min Long, Lei Zhao, Rong Jiang, Ke-Jian Wang, Shi-Fang Luo, Min Zheng, Xiao-Feng Li, Gui-Qiong H. Valproic Acid Modifies Synaptic Structure and Accelerates Neurite Outgrowth Via the Glycogen Synthase Kinase-3β Signaling Pathway in an Alzheimer's Disease Model. CNS neuroscience & therapeutics. vol 21. issue 11. 2016-07-22. PMID:26385876. tau hyperphosphorylation and amyloid β-peptide overproduction, caused by altered localization or abnormal activation of glycogen synthase kinase-3β (gsk-3β), is a pathogenic mechanism in alzheimer's disease (ad). 2016-07-22 2023-08-13 mouse
Xing Gao, Li Wang, Hai-Liang Huang, Lin-Lin Wang, Jun-Liang Yao, Shuo Shi, Tian-Ming Ya. Molecular "light switch" [Ru(phen)2dppzidzo](2+) monitoring the aggregation of tau. The Analyst. vol 140. issue 22. 2016-07-22. PMID:26460552. monitoring the aggregation of the tau protein is a key protocol for elucidating the pathogenic mechanism of alzheimer's disease. 2016-07-22 2023-08-13 Not clear
Jaspreet Kalra, Aamir Kha. Reducing Aβ load and tau phosphorylation: Emerging perspective for treating Alzheimer's disease. European journal of pharmacology. vol 764. 2016-07-21. PMID:26209363. reducing aβ load and tau phosphorylation: emerging perspective for treating alzheimer's disease. 2016-07-21 2023-08-13 Not clear
Louisa Mezache, Madison Mikhail, Michela Garofalo, Gerard J Nuov. Reduced miR-512 and the Elevated Expression of Its Targets cFLIP and MCL1 Localize to Neurons With Hyperphosphorylated Tau Protein in Alzheimer Disease. Applied immunohistochemistry & molecular morphology : AIMM. vol 23. issue 9. 2016-07-18. PMID:26258756. reduced mir-512 and the elevated expression of its targets cflip and mcl1 localize to neurons with hyperphosphorylated tau protein in alzheimer disease. 2016-07-18 2023-08-13 Not clear
Louisa Mezache, Madison Mikhail, Michela Garofalo, Gerard J Nuov. Reduced miR-512 and the Elevated Expression of Its Targets cFLIP and MCL1 Localize to Neurons With Hyperphosphorylated Tau Protein in Alzheimer Disease. Applied immunohistochemistry & molecular morphology : AIMM. vol 23. issue 9. 2016-07-18. PMID:26258756. the cause for the neurofibrillary tangles and plaques in alzheimer disease likely relates to an abnormal accumulation of their key components, which include β-amyloid and hyperphosphorylated tau protein. 2016-07-18 2023-08-13 Not clear
Louisa Mezache, Madison Mikhail, Michela Garofalo, Gerard J Nuov. Reduced miR-512 and the Elevated Expression of Its Targets cFLIP and MCL1 Localize to Neurons With Hyperphosphorylated Tau Protein in Alzheimer Disease. Applied immunohistochemistry & molecular morphology : AIMM. vol 23. issue 9. 2016-07-18. PMID:26258756. we segregated alzheimer brain sections from people with end-stage disease into those with abundant hyperphosphorylated tau protein and those without and compared each to normal brains for global microrna patterns. 2016-07-18 2023-08-13 Not clear
Louisa Mezache, Madison Mikhail, Michela Garofalo, Gerard J Nuov. Reduced miR-512 and the Elevated Expression of Its Targets cFLIP and MCL1 Localize to Neurons With Hyperphosphorylated Tau Protein in Alzheimer Disease. Applied immunohistochemistry & molecular morphology : AIMM. vol 23. issue 9. 2016-07-18. PMID:26258756. a significant reduced expression of several micrornas, including mir-512, was evident in the alzheimer brain sections with abundant hyperphosphorylated tau. 2016-07-18 2023-08-13 Not clear
Louisa Mezache, Madison Mikhail, Michela Garofalo, Gerard J Nuov. Reduced miR-512 and the Elevated Expression of Its Targets cFLIP and MCL1 Localize to Neurons With Hyperphosphorylated Tau Protein in Alzheimer Disease. Applied immunohistochemistry & molecular morphology : AIMM. vol 23. issue 9. 2016-07-18. PMID:26258756. mcm2 expression, a marker of neuroprogenitor cells, was significantly reduced in the alzheimer sections that contained the hyperphosphorylated tau. 2016-07-18 2023-08-13 Not clear
Louisa Mezache, Madison Mikhail, Michela Garofalo, Gerard J Nuov. Reduced miR-512 and the Elevated Expression of Its Targets cFLIP and MCL1 Localize to Neurons With Hyperphosphorylated Tau Protein in Alzheimer Disease. Applied immunohistochemistry & molecular morphology : AIMM. vol 23. issue 9. 2016-07-18. PMID:26258756. this, in turn, could lead to the accumulation of key alzheimer proteins such as hyperphosphorylated tau that ultimately prevent normal neuronal function and lead to disease symptomatology. 2016-07-18 2023-08-13 Not clear