ReviewNature neuroscience2015
Three dimensions of the amyloid hypothesis: time, space and 'wingmen'.
Review in Nature neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 376 papers, 3 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
376 citing papers in PubMed, 3 syntheses or guidelines pooled it, 691 citations in OpenAlex.
- Pooled it
- Neural stem/progenitor cell therapy for Alzheimer disease in preclinical rodent models: a systematic review and meta-analysis.Stem cell research & therapy · 2023Pooled it
- Herbal Therapeutics for Alzheimer's Disease: Ancient Indian Medicine System from the Modern Viewpoint.Current neuropharmacology · 2023Pooled it
- Tannic Acid Mitigates Monosodium Glutamate-Induced Cortical Damage by Modulating Synaptic and Calcium-Related Gene and Protein Expression.Journal of applied toxicology : JAT · 2026Article
- APOE3 and APOE4 human astrocytes differentially modulate Alzheimer's disease pathology and microglial responses in chimeric mice.Cell reports · 2026Article
- Amyloid precursor protein ortholog Appl acts with Vnd during mushroom body axon growth in Drosophila.Genetics · 2026Article
- Exploring and Targeting the Connection of Iron and Copper Homeostasis to Neurodegenerative Diseases.MedComm · 2026Review
- Abnormalities in core AD biomarkers precede inflammatory and glial markers in CSF in Autosomal Dominant Alzheimer's Disease.medRxiv : the preprint server for health sciences · 2026Article
- Zooming into Disease at the Nanoscale: High-Speed Atomic Force Microscopy in Biomedical Discovery.ACS nano · 2026Review
- Amyloid Beta Oligomers as Early Triggers of Neuronal Cytoskeleton Dysfunction in Alzheimer's Disease.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- Linking EEG markers of oscillopathy and default mode network dysfunction in Alzheimer's disease.Frontiers in human neuroscience · 2026Review
- Microglial clearance, neuroprotection and cognitive recovery via a novel synthetic sulfolipid in Alzheimer's disease.Journal of neuroinflammation · 2025Article
- Amyloid β Peptide Modifies Membrane Architecture and Surface Electrostatic Properties of Human Red Blood Cells.International journal of molecular sciences · 2025Article
- DKK3-LRP1 complex and a chemical inhibitor regulate Aβ clearance in models of Alzheimer's disease.Science advances · 2025Article
- Advancements in Stem Cell Research for Effective Therapies Against Alzheimer's Disease: Current Investigation and Future Insight.Molecular neurobiology · 2025Review
- Recent advances in the design, development and therapeutic applications of PPARγ agonists.Future medicinal chemistry · 2025Review
- Simultaneous EEG-PET-MRI identifies temporally coupled and spatially structured brain dynamics across wakefulness and NREM sleep.Nature communications · 2025Article
- REV-ERBα regulates brain NADNature aging · 2025Article
- APOE deficiency inhibits amyloid-facilitated (A) tau pathology (T) and neurodegeneration (N), halting progressive ATN pathology in a preclinical model.Molecular psychiatry · 2025Article
- Mendelian Randomization Reveals Unidirectional Links Between Amyloid-β and Tau in Alzheimer's Disease.Dementia and neurocognitive disorders · 2025Article
316 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 1 country.
Funding
Abstract
The amyloid hypothesis, which has been the predominant framework for research in Alzheimer's disease (AD), has been the source of considerable controversy. The amyloid hypothesis postulates that amyloid-β peptide (Aβ) is the causative agent in AD. It is strongly supported by data from rare autosomal dominant forms of AD. However, the evidence that Aβ causes or contributes to age-associated sporadic AD is more complex and less clear, prompting criticism of the hypothesis. We provide an overview of the major arguments for and against the amyloid hypothesis. We conclude that Aβ likely is the key initiator of a complex pathogenic cascade that causes AD. However, we argue that Aβ acts primarily as a trigger of other downstream processes, particularly tau aggregation, which mediate neurodegeneration. Aβ appears to be necessary, but not sufficient, to cause AD. Its major pathogenic effects may occur very early in the disease process.
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.