ReviewTranslational neurodegeneration2021
The role of pathological tau in synaptic dysfunction in Alzheimer's diseases.
Review in Translational neurodegeneration, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers, 3 of them syntheses that pooled it.
What it found
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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.
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Who cites it
145 citing papers in PubMed, 3 syntheses or guidelines pooled it, 217 citations in OpenAlex.
- Elevated temporal tau PET predicts faster cognitive decline in women than men: A meta-analysis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Pooled it
- Exploring easily accessible neurophysiological biomarkers for predicting Alzheimer's disease progression: a systematic review.Alzheimer's research & therapy · 2024Pooled it
- Glucagon-like peptide 1 (GLP-1) receptor agonists in experimental Alzheimer's disease models: a systematic review and meta-analysis of preclinical studies.Frontiers in pharmacology · 2023Pooled it
- Trial
- Elevation of the mechanically-sensitive e protein emerin links nuclear mechanotransduction to tau-induced cytoskeletal remodeling in neurons.Nucleus (Austin, Tex.) · 2026Article
- Simvastatin rescues cognitive impairment in an AβNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Fyn kinase: a key mechanistic regulator and therapeutic target in tauopathy and neurodegenerative diseases.Translational neurodegeneration · 2026Review
- From Dysbiosis to Blood-Brain Barrier Disruption: The Metabolite-Mediated Gut-Brain Axis in Alzheimer's Disease.Molecular neurobiology · 2026Review
- Tau Disaggregation by a CNS-Permeable Small Molecule Reduces Fibril and Oligomer Burden and Preserves Proteostasis and Behavior.bioRxiv : the preprint server for biology · 2026Article
- Trehalose's untapped mechanisms in alzheimer's: gut-brain-autophagy signalling beyond the usual targets.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026Review
- Tau-mediated Mechanisms in Alzheimer's Disease Pathogenesis.Molecular neurobiology · 2026Review
- Select microbial metabolites promote tau aggregation in a murine tauopathy model.Nature communications · 2026Article
- Vitamin K2 Promotes Mitochondrial Structural and Functional Homeostasis to Ameliorate Alzheimer Pathology by Targeting the EGFR-Ras-ERK Signaling Axis.International journal of molecular sciences · 2026Article
- Lymphoid-like Suppressive Microglia in Alzheimer's Disease: A New Neuroimmune Regulatory Axis?Cells · 2026Review
- Behavioral Complexity in Alzheimer's Disease: A Diversity-Based Analysis of Neuropsychiatric Symptoms.Brain sciences · 2026Article
- An Integrative Proteomic Approach to Reveal Altered Signaling Modules During Alzheimer's Disease Progression in PS19 Tauopathy Mice.Molecular & cellular proteomics : MCP · 2026Article
- Rhizomes as Multi-Target Pharmacological Platforms Against Tauopathy: Neuro-Metabolic Crosstalk, Drug-Likeness, and Translational Challenges.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Lipid metabolism, neuroinflammation, and oxidative stress in Alzheimer disease: an integrated mechanistic review.Acta neurologica Belgica · 2026Review
- Protective Effects of a Propolis-Journal of microbiology and biotechnology · 2026Article
- Signaling Pathways Triggering Therapeutical Potential of Marine-Derived Polysaccharides in Alzheimer's Disease: A Recent Review.Molecular neurobiology · 2026Review
85 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive cognitive decline, accompanied by amyloid-β (Aβ) overload and hyperphosphorylated tau accumulation in the brain. Synaptic dysfunction, an important pathological hallmark in AD, is recognized as the main cause of the cognitive impairments. Accumulating evidence suggests that synaptic dysfunction could be an early pathological event in AD. Pathological tau, which is detached from axonal microtubules and mislocalized into pre- and postsynaptic neuronal compartments, is suggested to induce synaptic dysfunction in several ways, including reducing mobility and release of presynaptic vesicles, decreasing glutamatergic receptors, impairing the maturation of dendritic spines at postsynaptic terminals, disrupting mitochondrial transport and function in synapses, and promoting the phagocytosis of synapses by microglia. Here, we review the current understanding of how pathological tau mediates synaptic dysfunction and contributes to cognitive decline in AD. We propose that elucidating the mechanism by which pathological tau impairs synaptic function is essential for exploring novel therapeutic strategies for AD.
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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.