ReviewNature2023
Molecular pathology of neurodegenerative diseases by cryo-EM of amyloids.
Review in Nature, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 157 papers.
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
157 citing papers in PubMed, 236 citations in OpenAlex.
- A murine model of amyloid-enhanced tauopathy: Comparison of wild-type and P301L-tau.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Repositioning of polyubiquitin alters the pathologic tau filament structure.Nature structural & molecular biology · 2026Article
- From aggregate structure to disease trajectory: the role of the proteostasis network.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Review
- Article
- Acoustofluidic cryo-EM enables in situ particle manipulation for uniform, high-quality cryo-EM specimens.Science advances · 2026Article
- Assembling peptides for treating Alzheimer's disease: a supramolecular perspective.RSC advances · 2026Review
- An N-terminal ATTR Fibril Segment Promotes Transthyretin Amyloid Nucleation and Polymorphism.bioRxiv : the preprint server for biology · 2026Article
- Neuroproteasomes regulate endogenous tau paired helical filament formation in an APOE genotype- and age-dependent manner.Nature neuroscience · 2026Article
- Tau Aggregate Imaging and Transcriptomics of Alzheimer's Disease Brain at Different Stages of Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Towards a systems-level view of the microtubule cytoskeleton and its functions in physiology and disease.Nature reviews. Molecular cell biology · 2026Review
- Cofactor-Free Tau Filaments Are Dynamic and Undergo Structural Evolution Driven by Thermodynamic Control.Journal of the American Chemical Society · 2026Article
- The Enigma of Big Tau Exon 4a: Genomic Architecture, Biophysical Identity, and Unique Evolutionary Mechanisms.Biomolecules · 2026Review
- α-Synuclein strain homogeneity in multiple system atrophy subtypes.Brain pathology (Zurich, Switzerland) · 2026Article
- Molecular Solution to the Paradox of Ancient Brain Preservation.Journal of proteome research · 2026Article
- Toward the prevention of clinically manifest Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
- Distinct amyloid-β filament fold in individuals with APP Flemish mutation.Nature structural & molecular biology · 2026Article
- The Pick fold in tau filaments from human MAPT mutants.Acta neuropathologica · 2026Article
- A scalable, dividing cell model for the robust propagation and quantification of human sporadic Creutzfeldt-Jakob disease prions.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- The amyloid packing difference: A pairwise comparison metric for amyloid structures.Structure (London, England : 1993) · 2026Article
- Thermodynamic Frontiers in Hemoglobin-Inspired Polymer Science for Diagnosis and Modulation of Neurodegenerative Diseases.Cell biochemistry and function · 2026Review
97 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
3 authors at 1 institution in 1 country.
Funding
Abstract
Abnormal assembly of tau, α-synuclein, TDP-43 and amyloid-β proteins into amyloid filaments defines most human neurodegenerative diseases. Genetics provides a direct link between filament formation and the causes of disease. Developments in cryo-electron microscopy (cryo-EM) have made it possible to determine the atomic structures of amyloids from postmortem human brains. Here we review the structures of brain-derived amyloid filaments that have been determined so far and discuss their impact on research into neurodegeneration. Whereas a given protein can adopt many different filament structures, specific amyloid folds define distinct diseases. Amyloid structures thus provide a description of neuropathology at the atomic level and a basis for studying disease. Future research should focus on model systems that replicate the structures observed in disease to better understand the molecular mechanisms of disease and develop improved diagnostics and therapies.
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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.