ReviewThe European journal of neuroscience2014
Tau acts as a mediator for Alzheimer's disease-related synaptic deficits.
Review in The European journal of neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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.
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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
28 citing papers in PubMed, 49 citations in OpenAlex.
- Amyloid-β, Tau Protein, α-Synuclein, TDP-43, and FUS in Mixed Pathology: And Intrinsic Disorder to Rule Them All.International journal of molecular sciences · 2026Review
- Concussive injuries induce neuronal stress-dependent tau mislocalization to dendritic spines with acrolein and functional network alteration in TBI-on-a-chip.Lab on a chip · 2025Article
- Multi-targeted approach via apigenin-7-O-glucoside for therapeutic intervention of Tau phosphorylating kinases in Alzheimer's disease.3 Biotech · 2025Article
- Acupuncture Ameliorates Alzheimer's-Like Cognitive Impairment and Pathological Changes via Regulating the Intestinal Fungal Community in APP/PS1 Mice.Neuropsychiatric disease and treatment · 2025Article
- Review
- Phospholipase D1 Attenuation Therapeutics Promotes Resilience against Synaptotoxicity in 12-Month-Old 3xTg-AD Mouse Model of Progressive Neurodegeneration.International journal of molecular sciences · 2023Article
- Role of Aβ in Alzheimer's-related synaptic dysfunction.Frontiers in cell and developmental biology · 2022Review
- Sex-Related Motor Deficits in the Tau-P301L Mouse Model.Biomedicines · 2021Article
- Orientation of neurites influences severity of mechanically induced tau pathology.Biophysical journal · 2021Article
- Dendritic spines are lost in clusters in Alzheimer's disease.Scientific reports · 2021Article
- Mechanical injuries of neurons induce tau mislocalization to dendritic spines and tau-dependent synaptic dysfunction.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Neuron Loss in Alzheimer's Disease: Translation in Transgenic Mouse Models.International journal of molecular sciences · 2020Review
- Biopharmaceutical Monotargeting versus 'Universal Targeting' of Late-Onset Alzheimer's Disease Using Mixtures of Pleiotropic Natural Compounds.Journal of Alzheimer's disease reports · 2019Review
- Inferior and medial temporal tau and cortical amyloid are associated with daily functional impairment in Alzheimer's disease.Alzheimer's research & therapy · 2019Article
- A53T Mutant Alpha-Synuclein Induces Tau-Dependent Postsynaptic Impairment Independently of Neurodegenerative Changes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- AD-Related N-Terminal Truncated Tau Is Sufficient to Recapitulate In Vivo the Early Perturbations of Human Neuropathology: Implications for Immunotherapy.Molecular neurobiology · 2018Article
- Amyloid, tau, pathogen infection and antimicrobial protection in Alzheimer's disease -conformist, nonconformist, and realistic prospects for AD pathogenesis.Translational neurodegeneration · 2018Review
- Genetic influences on cognition in progressive supranuclear palsy.Movement disorders : official journal of the Movement Disorder Society · 2017Article
- Sodium selenate regulates the brain ionome in a transgenic mouse model of Alzheimer's disease.Scientific reports · 2016Article
- Regional tau deposition measured by [Alzheimer's research & therapy · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The two histopathological hallmarks of Alzheimer's disease (AD) are amyloid plaques containing multiple forms of amyloid beta (Aβ) and neurofibrillary tangles containing phosphorylated tau proteins. As mild cognitive impairment frequently occurs long before the clinical diagnosis of AD, the scientific community has been increasingly interested in the roles of Aβ and tau in earlier cellular changes that lead to functional deficits. Therefore, great progress has recently been made in understanding how Aβ or tau causes synaptic dysfunction. However, the interaction between the Aβ and tau-initiated intracellular cascades that lead to synaptic dysfunction remains elusive. The cornerstone of the two-decade-old hypothetical amyloid cascade model is that amyloid pathologies precede tau pathologies. Although the premise of Aβ-tau pathway remains valid, the model keeps evolving as new signaling events are discovered that lead to functional deficits and neurodegeneration. Recent progress has been made in understanding Aβ-PrP(C) -Fyn-mediated neurotoxicity and synaptic deficits. Although still elusive, many novel upstream and downstream signaling molecules have been found to modulate tau mislocalization and tau hyperphosphorylation. Here we will discuss the mechanistic interactions between Aβ-PrP(C) -mediated neurotoxicity and tau-mediated synaptic deficits in an updated amyloid cascade model with calcium and tau as the central mediators.
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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.