ReviewNeuroscience bulletin2014
Tau-induced neurodegeneration: mechanisms and targets.
Review in Neuroscience bulletin, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
46 citing papers in PubMed.
- From nutrient-based to food-based assessment: the evolution of inflammatory indices and their significance for metabolic syndrome and type 3 diabetes mellitus.Frontiers in nutrition · 2026Review
- [Synapse (New York, N.Y.) · 2025Article
- Review
- Glucose enrichment reduces lifespan and promotes tau phosphorylation in human tau-expressing C. elegans, unaffected by O-β-GlcNAcylation induction.Journal of molecular medicine (Berlin, Germany) · 2025Article
- Evaluation of Alpha-Synuclein and Tau Antiaggregation Activity of Urea and Thiourea-Based Small Molecules for Neurodegenerative Disease Therapeutics.ACS chemical neuroscience · 2024Article
- P-tau217 as a Reliable Blood-Based Marker of Alzheimer's Disease.Biomedicines · 2024Review
- Mitophagy in Alzheimer's Disease: A Bibliometric Analysis from 2007 to 2022.Journal of Alzheimer's disease reports · 2024Article
- Death-associated protein kinase 1 is associated with cognitive dysfunction in major depressive disorder.Neural regeneration research · 2023Article
- Deregulated Transcription and Proteostasis in AdultInternational journal of molecular sciences · 2023Article
- Binding Parameters of [Pharmaceuticals (Basel, Switzerland) · 2023Article
- Insulin Deficiency Increases Sirt2 Level in Streptozotocin-Treated Alzheimer's Disease-Like Mouse Model: Increased Sirt2 Induces Tau Phosphorylation Through ERK Activation.Molecular neurobiology · 2022Article
- Optimal anti-amyloid-beta therapy for Alzheimer's disease via a personalized mathematical model.PLoS computational biology · 2022Article
- The Role of Post-Translational Modifications on the Structure and Function of Tau Protein.Journal of molecular neuroscience : MN · 2022Review
- Research trends of the neuroimaging in aphasia: A bibliometric analysis and visualization analysis from 2004 to 2021.Frontiers in human neuroscience · 2022Review
- The Clinical Significance of Cerebrospinal Fluid Reticulon 4 (RTN4) Levels in the Differential Diagnosis of Neurodegenerative Diseases.Journal of clinical medicine · 2021Article
- The Structure Biology of Tau and Clue for Aggregation Inhibitor Design.The protein journal · 2021Review
- Article
- Antisense Oligonucleotide-Mediated Reduction of HDAC6 Does Not Reduce Tau Pathology in P301S Tau Transgenic Mice.Frontiers in neurology · 2021Article
- The Crosstalk Between Pathological Tau Phosphorylation and Mitochondrial Dysfunction as a Key to Understanding and Treating Alzheimer's Disease.Molecular neurobiology · 2020Review
- Gold Nanoparticles Treatment Reverses Brain Damage in Alzheimer's Disease Model.Molecular neurobiology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
The accumulation of hyperphosphorylated tau is a common feature of several dementias. Tau is one of the brain microtubule-associated proteins. Here we discuss tau's functions in microtubule assembly and stabilization and with regard to its interactions with other proteins. We describe and analyze important post-translational modifications: hyperphosphorylation, ubiquitination, glycation, glycosylation, nitration, polyamination, proteolysis, acetylation, and methylation. We discuss how these post-translational modifications can alter tau's biological function. We analyze the role of mitochondrial health in neurodegeneration. We propose that microtubules could be a therapeutic target and review different approaches. Finally, we consider whether tau accumulation or its conformational change is related to tau-induced neurodegeneration, and propose a mechanism of neurodegeneration.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.