SynthesisFrontiers in neurology2020
Similarities and Differences in the Pattern of Tau Hyperphosphorylation in Physiological and Pathological Conditions: Impacts on the Elaboration of Therapies to Prevent Tau Pathology.
Synthesis in Frontiers in neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Salivary Biomarkers for Alzheimer's Disease: A Systematic Review with Meta-Analysis.International journal of molecular sciences · 2024Pooled it
- Selective degradation of DAPK1 via a novel hydrophobic tagging attenuates tau pathology in Alzheimer's disease.Journal of advanced research · 2026Article
- Toward nanomedicine-enabled RNA therapeutics for Alzheimer's disease.Molecular neurodegeneration advances · 2026Review
- Article
- Extracellular PHF-tau modulates astrocyte mitochondrial dynamics and mediates neuronal connectivity.Translational neurodegeneration · 2025Article
- Torpor induces reversible tau hyperphosphorylation and accumulation in mice expressing human tau.Acta neuropathologica communications · 2024Article
- Chronic Sustained Hypoxia Leads to Brainstem Tauopathy and Declines the Power of Rhythms in the Ventrolateral Medulla: Shedding Light on a Possible Mechanism.Molecular neurobiology · 2024Article
- Brain pathology and symptoms linked to concussion history: beyond chronic traumatic encephalopathy.Brain communications · 2024Article
- Recent insights from non-mammalian models of brain injuries: an emerging literature.Frontiers in neurology · 2024Review
- Current Challenges in the Diagnosis of Progressive Neurocognitive Disorders: A Critical Review of the Literature and Recommendations for Primary and Secondary Care.Brain sciences · 2023Review
- Interaction of Proteins Involved in Neuronal Proteinopathies.Life (Basel, Switzerland) · 2023Review
- Fiber-specific micro- and macroscopic white matter alterations in progressive supranuclear palsy and corticobasal syndrome.NPJ Parkinson's disease · 2023Article
- Tau pathology in neurodegenerative disease: disease mechanisms and therapeutic avenues.The Journal of clinical investigation · 2023Review
- Article
- 1-(7-Chloroquinolin-4-yl)-N-(4-Methoxybenzyl)-5-Methyl-1H-1,2, 3-Triazole-4- carboxamide Reduces Aβ Formation and Tau Phosphorylation in Cellular Models of Alzheimer's Disease.Neurochemical research · 2022Article
- Role of adipocyte Na,K-ATPase oxidant amplification loop in cognitive decline and neurodegeneration.iScience · 2021Article
- Ondine's Curse in Frontotemporal Dementia with Parkinsonism Linked to Chromosome 17 Caused byMovement disorders clinical practice · 2021Article
- P-tau231 as a Diagnostic Biomarker for Alzheimer's Disease and Mild Cognitive Impairment: A Systematic Review and Meta-Analysis.Annals of Indian Academy of NeurologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tau protein, a neuronal microtubule-associated protein, becomes hyperphosphorylated in several neurodegenerative diseases called tauopathies. Hyperphosphorylation of tau is correlated to its redistribution from the axon to the somato-dendritic compartment at early stages of tauopathies. Interestingly, tau hyperphosphorylation begins in different regions of the brain in each tauopathy. In some regions, both neurons and glial cells develop tau hyperphosphorylation. Tau hyperphosphorylation is also observed in physiological conditions such as hibernation and brain development. In the first section of present article, we will review the spatiotemporal and cellular distribution of hyperphosphorylated tau in the most frequent tauopathies. In the second section, we will compare the pattern of tau hyperphosphorylation in physiological and pathological conditions and discuss the sites that could play a pivotal role in the conversion of non-toxic to toxic forms of hyperphosphorylated tau. Furthermore, we will discuss the role of hyperphosphorylated tau in physiological and pathological conditions and the fact that tau hyperphosphorylation is reversible in physiological conditions but not in a pathological ones. In the third section, we will speculate how the differences and similarities between hyperphosphorylated tau in physiological and pathological conditions could impact the elaboration of therapies to prevent tau pathology. In the fourth section, the different therapeutic approaches using tau as a direct or indirect therapeutic target will be presented.
Indexed as
Identifiers
What OpenQuestion holds
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.