ReviewChinese medical journal2017
Tau-mediated Neurodegeneration and Potential Implications in Diagnosis and Treatment of Alzheimer's Disease.
Review in Chinese medical journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 75 citations in OpenAlex.
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- Photodynamic and Photothermal Therapies using Nanotechnology Approach in Alzheimer's Disease.Current neuropharmacology · 2025Review
- Understanding the Molecular Impact of Physical Exercise on Alzheimer's Disease.International journal of molecular sciences · 2024Review
- Recent advances in Alzheimer's disease: Mechanisms, clinical trials and new drug development strategies.Signal transduction and targeted therapy · 2024Review
- Autophagy in Disease Onset and Progression.Aging and disease · 2024Review
- Review
- Astaxanthin attenuates cognitive deficits in Alzheimer's disease models by reducing oxidative stress via the SIRT1/PGC-1α signaling pathway.Cell & bioscience · 2023Article
- Genetic Phenotypes of Alzheimer's Disease: Mechanisms and Potential Therapy.Phenomics (Cham, Switzerland) · 2023Review
- PINK1 overexpression prevents forskolin-induced tau hyperphosphorylation and oxidative stress in a rat model of Alzheimer's disease.Acta pharmacologica Sinica · 2022Article
- [5-Year Readmission Status and Risk Factors for Senile Dementia Patients: A Study Based on Chengdu Municipal Medical Insurance Database].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2022Article
- Plasma phosphorylated-tau181 levels reflect white matter microstructural changes across Alzheimer's disease progression.Metabolic brain disease · 2022Article
- Hypothesis on ontogenesis and pathophysiology of Alzheimer's disease.Einstein (Sao Paulo, Brazil) · 2022Review
- Roles and Mechanisms of the Protein Quality Control System in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Histological and imunohistochemical alterations of hippocampus and prefrontal cortex in a rat model of Alzheimer like-disease with a preferential role of the flavonoid "hesperidin".Journal of molecular histology · 2021Article
- Alteration of gene expression in reactive astrocytes induced by Aβ1-42 using low dose of methamphetamine.Molecular biology reports · 2021Article
- Imaging Techniques in Alzheimer's Disease: A Review of Applications in Early Diagnosis and Longitudinal Monitoring.International journal of molecular sciences · 2021Review
- Distribution of tau hyperphosphorylation in canine dementia resembles early Alzheimer's disease and other tauopathies.Brain pathology (Zurich, Switzerland) · 2021Article
- Delta-secretase triggers Alzheimer's disease pathologies in wild-type hAPP/hMAPT double transgenic mice.Cell death & disease · 2020Article
- Tau in Alzheimer's Disease: Pathological Alterations and an Attractive Therapeutic Target.Current medical science · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
objectiveTo review recent research advances on tau, a major player in Alzheimer's disease (AD) pathogenesis, a biomarker for AD onset, and potential target for AD therapy. DATA SOURCES: This review was based on a comprehensive search using online literature databases, including PubMed, Web of Science, and Google Scholar. STUDY SELECTION: Literature search was based on the following keywords: Alzheimer's disease, tau protein, biomarker, cerebrospinal fluid (CSF), therapeutics, plasma, imaging, propagation, spreading, seeding, prion, conformational templating, and posttranslational modification. Relevant articles were carefully reviewed, with no exclusions applied to study design and publication type.
resultsAmyloid plaques enriched with extracellular amyloid beta (Aβ) and intracellular neurofibrillary tangles comprised of hyperphosphorylated tau proteins are the two main pathological hallmarks of AD. Although the Aβ hypothesis has dominated AD research for many years, clinical Aβ-targeting strategies have consistently failed to effectively treat AD or prevent AD onset. The research focus in AD has recently shifted to the role of tau in AD. In addition to phosphorylation, tau is acetylated and proteolytically cleaved, which also contribute to its physiological and pathological functions. Emerging evidence characterizing pathological tau propagation and spreading provides new avenues for research into the molecular and cellular mechanisms underlying AD pathogenesis. Techniques to detect tau at minute levels in CSF and blood have been developed, and improved tracers have facilitated tau imaging in the brain. These advances have potential to accurately determine tau levels at early diagnostic stages in AD. Given that tau is a potential therapeutic target, anti-tau immunotherapy may potentially be a viable treatment strategy in AD intervention.
conclusionDetecting changes in tau and targeting tau pathology represent a promising lead in the diagnosis and treatment of AD.
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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.