ArticleInternational journal of Alzheimer's disease2012
Protein clearance mechanisms of alpha-synuclein and amyloid-Beta in lewy body disorders.
Article in International journal of Alzheimer's disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
The trial behind it
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- Cosolutes Modulate Polyubiquitin Fibrillation.ACS omega · 2026Article
- Plasma Autoantibodies Against Neurodegeneration-Related Antigens in Dementia and Elevated Chi3Li Autoantibodies in Mild Cognitive Impairment.Biomolecules · 2026Article
- Autoantibody profiles in Alzheimer´s, Parkinson´s, and dementia with Lewy bodies: altered IgG affinity and IgG/IgM/IgA responses to alpha-synuclein, amyloid-beta, and tau in disease-specific pathological patterns.Journal of neuroinflammation · 2024Article
- Exploring the Role of Hsp60 in Alzheimer's Disease and Type 2 Diabetes: Suggestion for Common Drug Targeting.International journal of molecular sciences · 2023Review
- Golgi Stress Response: New Insights into the Pathogenesis and Therapeutic Targets of Human Diseases.Molecules and cells · 2023Review
- Role of Astrocytes in Parkinson's Disease Associated with Genetic Mutations and Neurotoxicants.Cells · 2023Review
- Concomitant protein pathogenesis in Parkinson's disease and perspective mechanisms.Frontiers in aging neuroscience · 2023Review
- A Prospective Viewpoint on Neurological Diseases and Their Biomarkers.Molecules (Basel, Switzerland) · 2022Review
- Squalene-Based Nano-Assemblies Improve the Pro-Autophagic Activity of Trehalose.Pharmaceutics · 2022Article
- Bilirubin: A Promising Therapy for Parkinson's Disease.International journal of molecular sciences · 2021Review
- α-Synuclein modulates tau spreading in mouse brains.The Journal of experimental medicine · 2021Article
- Neurodegenerative diseases as proteinopathies-driven immune disorders.Neural regeneration research · 2020Review
- Impact of membrane curvature on amyloid aggregation.Biochimica et biophysica acta. Biomembranes · 2018Review
- Identification of a specific α-synuclein peptide (α-Syn 29-40) capable of eliciting microglial superoxide production to damage dopaminergic neurons.Journal of neuroinflammation · 2016Article
- Immunotherapeutic Approaches Targeting Amyloid-β, α-Synuclein, and Tau for the Treatment of Neurodegenerative Disorders.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2016Review
- Serotonin 1A Receptors on Astrocytes as a Potential Target for the Treatment of Parkinson's Disease.Current medicinal chemistry · 2016Review
- Progressive nigrostriatal terminal dysfunction and degeneration in the engrailed1 heterozygous mouse model of Parkinson's disease.Neurobiology of disease · 2015Article
- Accumulation of α-synuclein in dementia with Lewy bodies is associated with decline in the α-synuclein-degrading enzymes kallikrein-6 and calpain-1.Acta neuropathologica communications · 2014Article
- Augmentation of phenotype in a transgenic Parkinson mouse heterozygous for a Gaucher mutation.Brain : a journal of neurology · 2014Article
- Oxidative stress and neurodegenerative disorders.International journal of molecular sciences · 2013Review
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
No grant is acknowledged in the PubMed record.
Abstract
Protein clearance is critical for the maintenance of the integrity of neuronal cells, and there is accumulating evidence that in most-if not all-neurodegenerative disorders, impaired protein clearance fundamentally contributes to functional and structural alterations eventually leading to clinical symptoms. Dysfunction of protein clearance leads to intra- and extraneuronal accumulation of misfolded proteins and aggregates. The pathological hallmark of Lewy body disorders (LBDs) is the abnormal accumulation of misfolded proteins such as alpha-synuclein (Asyn) and amyloid-beta (Abeta) in a specific subset of neurons, which in turn has been related to deficits in protein clearance. In this paper we will highlight common intraneuronal (including autophagy and unfolded protein stress response) and extraneuronal (including interaction of neurons with astrocytes and microglia, phagocytic clearance, autoimmunity, cerebrospinal fluid transport, and transport across the blood-brain barrier) protein clearance mechanisms, which may be altered across the spectrum of LBDs. A better understanding of the pathways underlying protein clearance-in particular of Asyn and Abeta-in LBDs may result in the identification of novel biomarkers for disease onset and progression and of new therapeutic targets.
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.