ReviewJournal of cellular and molecular medicine2012
Interaction between pathogenic proteins in neurodegenerative disorders.
Review in Journal of cellular and molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 2 of them syntheses that pooled it.
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.
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
68 citing papers in PubMed, 2 syntheses or guidelines pooled it, 131 citations in OpenAlex.
- Diagnostic utility of GDF15 in neurodegenerative diseases: A systematic review and meta-analysis.Brain and behavior · 2022Pooled it
- The proteasome as a druggable target with multiple therapeutic potentialities: Cutting and non-cutting edges.Pharmacology & therapeutics · 2020Pooled it
- α-synuclein positivity is associated with decline in brain microstructure in the Alzheimer's disease spectrum.Alzheimer's research & therapy · 2026Article
- Morphological analysis of autophagy in axonal degeneration in gracile axonal dystrophy mice.Experimental animals · 2025Article
- An Emerging Prospective of Antipsychotics for Treating Neurodegenerative Disorders.Current pharmaceutical design · 2025Review
- Cerebrospinal fluid α-synuclein adds the risk of cognitive decline and is associated with tau pathology among non-demented older adults.Alzheimer's research & therapy · 2024Article
- Mild cognitive impairment in dementia with Lewy bodies: an update and outlook.Journal of neural transmission (Vienna, Austria : 1996) · 2023Review
- Connectome-based modelling of neurodegenerative diseases: towards precision medicine and mechanistic insight.Nature reviews. Neuroscience · 2023Review
- Cerebrospinal fluid alpha-synuclein, amyloid beta, total tau, and phosphorylated tau in tremor-dominant Parkinson's disease.Acta neurologica Belgica · 2023Article
- Morphological characteristics differentiate dementia with Lewy bodies from Parkinson disease with and without dementia.Journal of neural transmission (Vienna, Austria : 1996) · 2023Article
- Employing nanoparticle tracking analysis of salivary neuronal exosomes for early detection of neurodegenerative diseases.Translational neurodegeneration · 2023Review
- Potential of Therapeutic Small Molecules in Apoptosis Regulation in the Treatment of Neurodegenerative Diseases: An Updated Review.Molecules (Basel, Switzerland) · 2022Review
- Impact of Heat Shock Proteins in Neurodegeneration: Possible Therapeutical Targets.Annals of neurosciences · 2022Review
- Descriptive Epidemiology of Neurodegenerative Diseases: What Are the Critical Questions?Neuroepidemiology · 2022Article
- A Possible Role for HMG-CoA Reductase Inhibitors and Its Association withInternational journal of molecular sciences · 2021Review
- αS Oligomers Generated from Interactions with a Polyunsaturated Fatty Acid and a Dopamine Metabolite Differentially Interact with Aβ to Enhance Neurotoxicity.ACS chemical neuroscience · 2021Article
- Distribution of α-synuclein in normal human jejunum and its relations with the chemosensory and neuroendocrine system.European journal of histochemistry : EJH · 2021Article
- 1,5-Benzodiazepin-2(3H)-ones: In Vitro Evaluation as Antiparkinsonian Agents.Antioxidants (Basel, Switzerland) · 2021Article
- Understanding Amyloid Structures and Disease: A Continuing Challenge in Health Research.International journal of molecular sciences · 2021Article
- Significance of cerebral amyloid angiopathy and other co-morbidities in Lewy body diseases.Journal of neural transmission (Vienna, Austria : 1996) · 2021Article
8 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
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The misfolding and progressive aggregation of specific proteins in selective regions of the nervous system is a seminal occurrence in many neurodegenerative disorders, and the interaction between pathological/toxic proteins to cause neurodegeneration is a hot topic of current neuroscience research. Despite clinical, genetic and experimental differences, increasing evidence indicates considerable overlap between synucleinopathies, tauopathies and other protein-misfolding diseases. Inclusions, often characteristic hallmarks of these disorders, suggest interactions of pathological proteins enganging common downstream pathways. Novel findings that have shifted our understanding in the role of pathologic proteins in the pathogenesis of Alzheimer, Parkinson, Huntington and prion diseases, have confirmed correlations/overlaps between these and other neurodegenerative disorders. Emerging evidence, in addition to synergistic effects of tau protein, amyloid-β, α-synuclein and other pathologic proteins, suggests that prion-like induction and spreading, involving secreted proteins, are major pathogenic mechanisms in various neurodegenerative diseases, depending on genetic backgrounds and environmental factors. The elucidation of the basic molecular mechanisms underlying the interaction and spreading of pathogenic proteins, suggesting a dualism or triad of neurodegeneration in protein-misfolding disorders, is a major challenge for modern neuroscience, to provide a deeper insight into their pathogenesis as a basis of effective diagnosis and treatment.
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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.