ReviewNature reviews. Neurology2013
Alzheimer disease therapy--moving from amyloid-β to tau.
Review in Nature reviews. Neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 223 papers, 4 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
223 citing papers in PubMed, 4 syntheses or guidelines pooled it, 474 citations in OpenAlex.
- Targeting Protein Aggregates with Natural Products: An Optional Strategy for Neurodegenerative Diseases.International journal of molecular sciences · 2023Pooled it
- Association between Apolipoprotein E Gene Polymorphism and Alzheimer's Disease in an Iranian Population: A Meta-Analysis.Journal of molecular neuroscience : MN · 2019Pooled it
- Cognitive Decline in Preclinical Alzheimer's Disease: Amyloid-Beta versus Tauopathy.Journal of Alzheimer's disease : JAD · 2018Pooled it
- The associations between the MAPT polymorphisms and Alzheimer's disease risk: a meta-analysis.Oncotarget · 2017Pooled it
- Dual Targeted Far-Red Emissive Small Molecules for Mitochondrial Imaging and Multifunctional Modulation in Alzheimer's Disease.Advanced healthcare materials · 2026Article
- Latent brain state dynamics predict early amyloid accumulation and cognitive impairment.bioRxiv : the preprint server for biology · 2026Article
- Modeling and application of alzheimer's disease complex trait prediction based on multi-task learning.Scientific reports · 2026Article
- Pharmacological Characterization ofRecent advances in inflammation & allergy drug discovery · 2026Article
- Intervention of ginseng-derived macromolecular drugs in Alzheimer's disease: exploring mechanisms and assessing potential.Frontiers in aging neuroscience · 2026Review
- Synergistic Neuroprotection in Tauopathic Mice via Green-Synthesized Silver Nanoparticles Co-delivering Methylene Blue and Moringa oleifera.Molecular neurobiology · 2025Article
- Caenorhabditis Elegans Ortholog of TNF Alpha-Induced Protein 1 is Upregulated by TOL-1 and Exacerbates Amyloid-Beta-Associated Pathology.Molecular neurobiology · 2025Article
- Calcium signaling hypothesis: A non-negligible pathogenesis in Alzheimer's disease.Journal of advanced research · 2025Review
- Research trends of piezoelectric materials in neurodegenerative disease applications.Bioactive materials · 2025Review
- Brain tau PET-based identification and characterization of subpopulations in patients with Alzheimer's disease using deep learning-derived saliency maps.EJNMMI physics · 2025Article
- Morphological and Molecular Profiling of Amyloid-β Species in Alzheimer's Pathogenesis.Molecular neurobiology · 2025Review
- The Role of the Urea Cycle in the Alzheimer's Disease Brain.Journal of neurochemistry · 2025Review
- Clinical-grade human dental pulp stem cells improve adult hippocampal neural regeneration and cognitive deficits in Alzheimer's disease.Theranostics · 2025Article
- A Review on Nanotechnology basedCNS & neurological disorders drug targets · 2025Review
- Alzheimer's Disease Protein Targets: Comprehensive Review and Future Directions.Current pharmaceutical design · 2025Review
- Hippocampal GPR35 Participates in the Pathogenesis of Cognitive Deficits and Emotional Alterations Induced by AβMolecular neurobiology · 2025Article
163 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
2 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Disease-modifying treatments for Alzheimer disease (AD) have focused mainly on reducing levels of amyloid-β (Aβ) in the brain. Some compounds have achieved this goal, but none has produced clinically meaningful results. Several methodological issues relating to clinical trials of these agents might explain this failure; an additional consideration is that the amyloid cascade hypothesis--which places amyloid plaques at the heart of AD pathogenesis--does not fully integrate a large body of data relevant to the emergence of clinical AD. Importantly, amyloid deposition is not strongly correlated with cognition in multivariate analyses, unlike hyperphosphorylated tau, neurofibrillary tangles, and synaptic and neuronal loss, which are closely associated with memory deficits. Targeting tau pathology, therefore, might be more clinically effective than Aβ-directed therapies. Furthermore, numerous immunization studies in animal models indicate that reduction of intracellular levels of tau and phosphorylated tau is possible, and is associated with improved cognitive performance. Several tau-related vaccines are in advanced preclinical stages and will soon enter clinical trials. In this article, we present a critical analysis of the failure of Aβ-directed therapies, discuss limitations of the amyloid cascade hypothesis, and suggest the potential value of tau-targeted therapy 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.