ReviewJournal of Alzheimer's disease : JAD2018
Role of Amyloid-β and Tau Proteins in Alzheimer's Disease: Confuting the Amyloid Cascade.
Review in Journal of Alzheimer's disease : JAD, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 169 papers, 2 of them syntheses 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
169 citing papers in PubMed, 2 syntheses or guidelines pooled it, 276 citations in OpenAlex.
- Efficacy of antioxidants as a therapy for Alzheimer's disease: a meta-analysis.Frontiers in nutrition · 2026Pooled it
- The Role of Protein Misfolding and Tau Oligomers (TauOs) in Alzheimer's Disease (AD).International journal of molecular sciences · 2019Pooled it
- Review
- APOE4-AGE axis is linked to mtDNA release and cGAS-STING-mediated neuroinflammation in the aging brain.Free radical biology & medicine · 2026Article
- Prediction of mild cognitive impairment progression using time-sensitive multimodal biomarkers.Science advances · 2026Article
- The mitochondrial unfolded protein response in human microglia disrupts neuronal-glial communication and promotes senescence.Nature neuroscience · 2026Article
- iPSC-Derived 3D Brain Organoids as Next-generation Platforms to Study Viral and Toxicant-associated Neurodegeneration.Stem cell reviews and reports · 2026Review
- TREM2 in neurodegeneration and diseases.Molecular psychiatry · 2026Review
- Putatively Identified Sarmentoside-B Removes Oligomerized Amyloid Peptide from Neurons by Inhibiting mTOR and Restoring Lysosomal Function, in In Vitro Alzheimer's Disease Model.Pharmaceutics · 2026Article
- A metabolite extracted from Escherichia coli suppresses tau aggregation.The Biochemical journal · 2026Article
- GGAs: Regulation of Multiple Sorting Pathways and Potential Association With Human Diseases.Journal of cellular and molecular medicine · 2026Review
- Plant-mediated green nanoparticles: combining nanometal and biometabolite potential for Alzheimer's treatment.Biomedical engineering online · 2026Review
- Chrysin Ameliorated Neurochemical and Behavioural Changes Mediated By Combined Exposure of Interleukin-17 A With Amyloid BetaJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Article
- Artificial intelligence and multiomics integration for Parkinson's disease drug development.Molecules and cells · 2026Review
- 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
- Integrating ensemble machine-learning and fibril docking to discover potent, novel triazole-naphthalene tau-aggregation inhibitors.Molecular diversity · 2026Article
- Metabolic Dysfunction in Alzheimer's Disease: Brain Glucose Hypometabolism as an Early Precursor to Amyloid and Tau Pathology.Journal of clinical medicine · 2026Review
- Mesenchymal Stem Cell-Based Therapies Applied in Neurological Diseases: A Systematic Review.Biomedicines · 2026Review
- Cognitive Decline and Neurodegenerative Markers in Psoriasis: The Role of APOE4 and Beta-Amyloid.Dermatology practical & conceptual · 2026Article
- The Molecular Architecture of Neurodegeneration: An Integrative Overview of Convergent Mechanisms.NeuroSci · 2026Review
109 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
Abstract
The "Amyloid Cascade Hypothesis" has dominated the Alzheimer's disease (AD) field in the last 25 years. It posits that the increase of amyloid-β (Aβ) is the key event in AD that triggers tau pathology followed by neuronal death and eventually, the disease. However, therapeutic approaches aimed at decreasing Aβ levels have so far failed, and tau-based clinical trials have not yet produced positive findings. This begs the question of whether the hypothesis is correct. Here we have examined literature on the role of Aβ and tau in synaptic dysfunction, memory loss, and seeding and spreading of AD, highlighting important parallelisms between the two proteins in all of these phenomena. We discuss novel findings showing binding of both Aβ and tau oligomers to amyloid-β protein precursor (AβPP), and the requirement for the presence of this protein for both Aβ and tau to enter neurons and induce abnormal synaptic function and memory. Most importantly, we propose a novel view of AD pathogenesis in which extracellular oligomers of Aβ and tau act in parallel and upstream of AβPP. Such a view will call for a reconsideration of therapeutic approaches directed against Aβ and tau, paving the way to an increased interest toward AβPP, both for understanding the pathogenesis of the disease and elaborating new therapeutic strategies.
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.