ReviewCell & bioscience2021
α-Synuclein-mediated neurodegeneration in Dementia with Lewy bodies: the pathobiology of a paradox.
Review in Cell & bioscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 26 citations in OpenAlex.
- PROTAC-Based Strategies in Neurodegenerative Diseases: Challenges and Perspectives.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Molecular Crossroads: Shared and Divergent Molecular Signatures in Alzheimer's Disease and Dementia with Lewy Bodies.International journal of molecular sciences · 2025Review
- A Causal Association Between Drug Use and Cognitive Impairment: A Two-Sample Mendelian Randomization Study.Brain and behavior · 2025Article
- The Therapeutic Potential of Dietary Phytochemicals in Age-Related Neurodegenerative Disorders.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Seed Amplification Assay for α-Synuclein: Diagnostic Applications in Synucleinopathies.International journal of molecular sciences · 2025Review
- Synapse vulnerability and resilience across the clinical spectrum of dementias.Nature reviews. Neurology · 2025Review
- Advancements in PROTAC-based therapies for neurodegenerative diseases.Future medicinal chemistry · 2025Review
- Protective Effects of Ambroxol on Aβ and α-Synuclein-Induced Neurotoxicity Through Glucocerebrosidase Activation in HT-22 Hippocampal Neuronal Cells.International journal of molecular sciences · 2024Article
- Targeted protein degradation: advances in drug discovery and clinical practice.Signal transduction and targeted therapy · 2024Review
- Modeling Lewy body disease withScience advances · 2024Article
- Unlocking the Potential: Semaglutide's Impact on Alzheimer's and Parkinson's Disease in Animal Models.Current issues in molecular biology · 2024Review
- Grey matter networks in women and men with dementia with Lewy bodies.NPJ Parkinson's disease · 2024Article
- Toward Personalized Medicine Approaches for Parkinson Disease Using Digital Technologies.JMIR formative research · 2023Review
- Kisspeptin-10 Mitigates α-Synuclein-Mediated Mitochondrial Apoptosis in SH-SY5Y-Derived Neurons via a Kisspeptin Receptor-Independent Manner.International journal of molecular sciences · 2023Article
- Alpha synuclein post translational modifications: potential targets for Parkinson's disease therapy?Frontiers in molecular neuroscience · 2023Review
- Kisspeptin-10 Rescues Cholinergic Differentiated SHSY-5Y Cells from α-Synuclein-Induced Toxicity In Vitro.International journal of molecular sciences · 2022Article
- In Pancreatic Adenocarcinoma Alpha-Synuclein Increases and Marks Peri-Neural Infiltration.International journal of molecular sciences · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dementia with Lewy bodies (DLB) is epitomized by the pathognomonic manifestation of α-synuclein-laden Lewy bodies within selectively vulnerable neurons in the brain. By virtue of prion-like inheritance, the α-synuclein protein inexorably undergoes extensive conformational metamorphoses and culminate in the form of fibrillar polymorphs, instigating calamitous damage to the brain's neuropsychological networks. This epiphenomenon is nebulous, however, by lingering uncertainty over the quasi "pathogenic" behavior of α-synuclein conformers in DLB pathobiology. Despite numerous attempts, a monolithic "α-synuclein" paradigm that is able to untangle the enigma enshrouding the clinicopathological spectrum of DLB has failed to emanate. In this article, we review conceptual frameworks of α-synuclein dependent cell-autonomous and non-autonomous mechanisms that are likely to facilitate the transneuronal spread of degeneration through the neuraxis. In particular, we describe how the progressive demise of susceptible neurons may evolve from cellular derangements perpetrated by α-synuclein misfolding and aggregation. Where pertinent, we show how these bona fide mechanisms may mutually accentuate α-synuclein-mediated neurodegeneration in the DLB brain.
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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.