ReviewTrends in molecular medicine2020
Cell-to-Cell Transmission of Tau and α-Synuclein.
Review in Trends in molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.
What it found
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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
102 citing papers in PubMed.
- The MR1/MAIT cell axis has limited effects on the start of tau pathology in a mouse model of tauopathy.Brain, behavior, and immunity · 2026Article
- Development of an RNA aptamer as a therapeutic agent for synucleinopathies.Nature communications · 2026Article
- Distinct Molecular Mechanisms Underlie Modulation of Seeded α-Synuclein Aggregation and Toxicity by Salvianolic Acid B and Dihydromyricetin.International journal of molecular sciences · 2026Article
- Brain atrophy patterns in anti-IgLON5 disease.Brain : a journal of neurology · 2026Article
- HDAC6 Inhibition Reduces Seeded Tau and α-Synuclein Pathologies in Primary Neuron Cultures and Wild-Type Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Hidden faces of alpha-synuclein: Cryo-EM revelation of fibril polymorphs driven by disease, mutations, and PTMs.BBA advances · 2026Review
- Exidavnemab binds to aggregated α-synuclein in human brains affected by α-synucleinopathies.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Propagation of α-synuclein pathology: models, mechanisms and future goals.Molecular neurodegeneration advances · 2026Review
- Differential microglial responses to structurally distinct alpha-synuclein polymorphs.Molecular brain · 2025Article
- Direct interaction between TDP-43 and Tau promotes their co-condensation, while suppressing Tau fibril formation and seeding.The EMBO journal · 2025Article
- Activated microglial exosomes enhance α-Synuclein internalization and accelerate neurodegeneration in lewy body dementia.Journal of nanobiotechnology · 2025Article
- Brain and retina in Alzheimer's disease: Pathological intersections and estimates from imaging.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Blood α-Synuclein Separates Parkinson's Disease from Dementia with Lewy Bodies.Annals of neurology · 2025Article
- Beyond the Secretory Pathway: New Insights Into Protein Release.Traffic (Copenhagen, Denmark) · 2025Review
- Intercellular propagation of RIPK1/RIPK3 amyloid fibrils.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Progress in Disease-Modifying Therapies for Parkinson's Disease.Aging and disease · 2025Review
- Lysine-Targeting Inhibitors of Amyloidogenic Protein Aggregation: A Promise for Neurodegenerative Proteinopathies.JACS Au · 2025Review
- Design of Ig-like binders targeting α-synuclein fibril for mitigating its pathological activities.Nature communications · 2025Article
- Recent Advances in Autophagy and Immunotherapy for the Clearance of Aggregated α-Synuclein in Parkinson's Disease.Aging and disease · 2025Review
- Reply: PART and amyloid cascade hypotheses are alive and well (but are not so simple).Acta neuropathologica · 2025Article
42 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
5 authors.
Funding
Abstract
The stereotypical spread of pathological protein inclusions and clinicopathological heterogeneity are well described in neurodegenerative diseases. Accumulating evidence suggests that the former can be attributed to consecutive cell-to-cell transmission of pathological proteins between anatomically connected brain regions, while the latter has been hypothesized to result from the spread of conformationally distinct pathological protein aggregates, or strains. These emerging concepts have dramatically changed our understanding of neurodegenerative diseases. In this review, we first summarize the background and recent findings underpinning these concepts with a focus on two major pathological proteins: tau and α-synuclein. We then discuss their clinical implications for tauopathies and synucleinopathies and propose a working hypothesis for future research.
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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.