ArticleNeurobiology of disease2017
Differential effects of immunotherapy with antibodies targeting α-synuclein oligomers and fibrils in a transgenic model of synucleinopathy.
Article in Neurobiology of disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 45 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
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
45 citing papers in PubMed, 85 citations in OpenAlex.
- Quantitative systems pharmacology model of α-synuclein pathology in Parkinson's disease-like mouse for investigation of passive immunotherapy mechanisms.CPT: pharmacometrics & systems pharmacology · 2024Article
- Review
- α-Synuclein oligomers potentiate neuroinflammatory NF-κB activity and induce CaTranslational neurodegeneration · 2024Article
- Brain-Targeted Liposomes Loaded with Monoclonal Antibodies Reduce Alpha-Synuclein Aggregation and Improve Behavioral Symptoms in Parkinson's Disease.Advanced materials (Deerfield Beach, Fla.) · 2023Article
- A functional role for alpha-synuclein in neuroimmune responses.Journal of neuroimmunology · 2023Review
- A Mouse Model to Test Novel Therapeutics for Parkinson's Disease: an Update on the Thy1-aSyn ("line 61") Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Aging exacerbates the brain inflammatory micro-environment contributing to α-synuclein pathology and functional deficits in a mouse model of DLB/PD.Molecular neurodegeneration · 2022Article
- Novel engineered nanobodies specific for N-terminal region of alpha-synuclein recognize Lewy-body pathology and inhibit in-vitro seeded aggregation and toxicity.The FEBS journal · 2022Article
- Conformation-specific Antibodies Targeting Aggregated Forms of α-synuclein Block the Propagation of Synucleinopathy.Experimental neurobiology · 2022Article
- Passive Immunization in Alpha-Synuclein Preclinical Animal Models.Biomolecules · 2022Review
- Efficacy and immunogenicity of MultiTEP-based DNA vaccines targeting human α-synuclein: prelude for IND enabling studies.NPJ vaccines · 2022Article
- Alpha-Synuclein Targeting Therapeutics for Parkinson's Disease and Related Synucleinopathies.Frontiers in neurology · 2022Review
- Toward a Disease-Modifying Therapy of Alpha-Synucleinopathies: New Molecules and New Approaches Came into the Limelight.Molecules (Basel, Switzerland) · 2021Review
- Current experimental disease-modifying therapeutics for multiple system atrophy.Journal of neural transmission (Vienna, Austria : 1996) · 2021Review
- Roles of α‑synuclein in gastrointestinal microbiome dysbiosis‑related Parkinson's disease progression (Review).Molecular medicine reports · 2021Review
- Alpha-synuclein research: defining strategic moves in the battle against Parkinson's disease.NPJ Parkinson's disease · 2021Review
- Exploring the Release of Toxic Oligomers from α-Synuclein Fibrils with Antibodies and STED Microscopy.Life (Basel, Switzerland) · 2021Article
- The Contribution of Microglia to Neuroinflammation in Parkinson's Disease.International journal of molecular sciences · 2021Review
- Periphery and brain, innate and adaptive immunity in Parkinson's disease.Acta neuropathologica · 2021Review
- LRRK2 Kinase Inhibitor Rejuvenates Oxidative Stress-Induced Cellular Senescence in Neuronal Cells.Oxidative medicine and cellular longevity · 2021Article
Corrections and comments
- Retraction · 2025-01-15Concerns/Issues about Image · Duplication of/in Image · Error in Image · Investigation by Journal/Publisher · Investigation by Third Party · Unreliable Image · · see also: https://pubpeer.com/publications/E8BFBC4D110BB705D8152DA8AAD90D
- Retracted
Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
Abstract
Disorders with progressive accumulation of α-synuclein (α-syn) are a common cause of dementia and parkinsonism in the aging population. Accumulation and propagation of α-syn play a role in the pathogenesis of these disorders. Previous studies have shown that immunization with antibodies that recognize C-terminus of α-syn reduces the intra-neuronal accumulation of α-syn and related deficits in transgenic models of synucleinopathy. These studies employed antibodies that recognize epitopes within monomeric and aggregated α-syn that were generated through active immunization or administered via passive immunization. However, it is possible that more specific effects might be achieved with antibodies recognizing selective species of the α-syn aggregates. In this respect we recently developed antibodies that differentially recognized various oligomers (Syn-O1, -O2, and -O4) and fibrilar (Syn-F1 and -F2) forms of α-syn. For this purpose wild-type α-syn transgenic (line 61) mice were immunized with these 5 different antibodies and neuropathologically and biochemically analyzed to determine which was most effective at reducing α-syn accumulation and related deficits. We found that Syn-O1, -O4 and -F1 antibodies were most effective at reducing accumulation of α-syn oligomers in multiple brain regions and at preventing neurodegeneration. Together this study supports the notion that selective antibodies against α-syn might be suitable for development new treatments for synucleinopathies such as PD and DLB.
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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.