ReviewThe Journal of biological chemistry2012
Corruption and spread of pathogenic proteins in neurodegenerative diseases.
Review in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed.
- Direct Observation of Secondary Nucleation in Huntingtin Amyloid Formation by High-Speed Atomic Force Microscopy.Journal of the American Chemical Society · 2025Article
- In Vivo Seeding of Amyloid-β Protein and Implications in Modeling Alzheimer's Disease Pathology.Biomolecules · 2025Review
- Current limitations and future opportunities of tracer studies of muscle ageing.The Journal of physiology · 2025Article
- Do Bacterial Outer Membrane Vesicles Contribute to Chronic Inflammation in Parkinson's Disease?Journal of Parkinson's disease · 2024Review
- Minimal mechanistic component of HbYX-dependent proteasome activation that reverses impairment by neurodegenerative-associated oligomers.Communications biology · 2023Article
- Ovarian Cancer and Parkinson's Disease: A Bidirectional Mendelian Randomization Study.Journal of clinical medicine · 2023Article
- Minimal mechanistic component of HbYX-dependent proteasome activation.Research square · 2023Article
- Graph Models of Pathology Spread in Alzheimer's Disease: An Alternative to Conventional Graph Theoretic Analysis.Brain connectivity · 2021Review
- Protofilament Structure and Supramolecular Polymorphism of Aggregated Mutant Huntingtin Exon 1.Journal of molecular biology · 2020Article
- Aggregation and Prion-Inducing Properties of the G-Protein Gamma Subunit Ste18 are Regulated by Membrane Association.International journal of molecular sciences · 2020Article
- Molecular crosstalk between cancer and neurodegenerative diseases.Cellular and molecular life sciences : CMLS · 2020Review
- Effects of Physical Exercise on Autophagy and Apoptosis in Aged Brain: Human and Animal Studies.Frontiers in nutrition · 2020Review
- Proteostasis collapse is a driver of cell aging and death.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Neurotheranostics as personalized medicines.Advanced drug delivery reviews · 2019Review
- Biomarkers for tau pathology.Molecular and cellular neurosciences · 2019Review
- Sequence features governing aggregation or degradation of prion-like proteins.PLoS genetics · 2018Article
- Small-molecule PET Tracers for Imaging Proteinopathies.Seminars in nuclear medicine · 2017Review
- Journey of cystatins from being mere thiol protease inhibitors to at heart of many pathological conditions.International journal of biological macromolecules · 2017Review
- Prion-based memory of heat stress in yeast.Prion · 2017Article
- Yeast Short-Lived Actin-Associated Protein Forms a Metastable Prion in Response to Thermal Stress.Cell reports · 2017Article
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.
Funding
Abstract
With advancing age, the brain becomes increasingly susceptible to neurodegenerative diseases, most of which are characterized by the misfolding and errant aggregation of certain proteins. The induction of aggregation involves a crystallization-like seeding mechanism by which a specific protein is structurally corrupted by its misfolded conformer. The latest research indicates that, once formed, proteopathic seeds can spread from one locale to another via cellular uptake, transport, and release. Impeding this process could represent a unified therapeutic strategy for slowing the progression of a wide range of currently intractable disorders.
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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.