ArticleActa neuropathologica communications2022
Discrepancy between distribution of alpha-synuclein oligomers and Lewy-related pathology in Parkinson's disease.
Article in Acta neuropathologica communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 57 citations in OpenAlex.
- The 201 Trial: a placebo-controlled randomized phase 2 study of safety and tolerance of the c-Abl kinase inhibitor risvodetinib in untreated Parkinson's disease.Nature aging · 2026Trial
- Etiology and therapeutics for cognitive dysfunction in multiple system atrophy.Neural regeneration research · 2026Article
- Seeing Invisible Oligomers: Rethinking α-Synuclein Pathology Through Proximity Ligation Assay.Movement disorders : official journal of the Movement Disorder Society · 2026Review
- Large-scale visualization of α-synuclein oligomers in Parkinson's disease brain tissue.Nature biomedical engineering · 2026Article
- Molecular profiling of alpha-synuclein pathology and seeding activity in Parkinson's disease.Acta neuropathologica · 2026Article
- Neuropathologic basis of quantitative susceptibility mapping in the substantia nigra: contributions of tau, pigmented neurons, and iron.Acta neuropathologica · 2026Article
- Clinical Validation of α-Synuclein in Salivary Extracellular Vesicles as a Biomarker for Parkinson's Disease: A Longitudinal Study.European journal of neurology · 2026Article
- Mapping cellular vulnerability in Parkinson's disease using retro-AAVs and preformed α-synuclein fibrils.Translational neurodegeneration · 2026Article
- Exidavnemab binds to aggregated α-synuclein in human brains affected by α-synucleinopathies.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Long-term oral glucocerebrosidase activator reduces soluble α-synuclein oligomer accumulation in Parkinsonian LRRK2 mutant mouse brain.NPJ Parkinson's disease · 2025Article
- Longitudinal insights from iron accumulation in motor system of prodromal and clinical Parkinson's disease.NPJ Parkinson's disease · 2025Article
- Alpha-Synuclein Neurobiology in Parkinson's Disease: A Comprehensive Review of Its Role, Mechanisms, and Therapeutic Perspectives.Brain sciences · 2025Review
- Are we ready for a biological diagnosis of Parkinson's Disease?Cell death & disease · 2025Review
- Neuropathology of Lewy body dementia: Lewy-related pathology, α-synuclein oligomers, and comorbid pathologies.Molecular neurodegeneration · 2025Review
- Converging pathologies in neurodegeneration: the mechanistic interplay between α-Synuclein and Tau in Alzheimer's and Parkinson's.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Review
- Facilitated α-synuclein oligomer sharing among glial cells by a centrally acting connexin inhibitor attenuates a rapidly progressive multiple system atrophy-cerebellar type model by reducing the neuronal α-synuclein burden.Acta neuropathologica communications · 2025Article
- Impact of hippocampal α-synuclein oligomers on cognitive trajectory in patients with dementia with Lewy bodies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Immunization targeting diseased proteins in synucleinopathy and tauopathy: insights from clinical trials.Translational neurodegeneration · 2025Review
- Current strategies in the management of dementia with lewy bodies and future directions based on disease pathophysiology.Molecular neurodegeneration · 2025Review
- Abundant non-inclusion α-synuclein pathology in Lewy body-negative LRRK2-mutant cases.Acta neuropathologica · 2025Article
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Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathological hallmarks of Parkinson's disease (PD) are α-synuclein (αSYN)-positive inclusions referred to as Lewy bodies and Lewy neurites, collectively referred to as Lewy-related pathology (LRP). LRP is thought to propagate in an ascending manner throughout the brain as the disease progresses. LRP is visible with histologic methods and is thought to represent a later stage of the disease process, while αSYN oligomers, which are not visible with routine histologic methods, are considered earlier. There is increasing evidence to suggest that αSYN oligomers may be more toxic than visible LRP. Detecting αSYN oligomers requires special techniques, and their distribution and association with clinical features are important research objectives. In this report, we describe the distribution of αSYN oligomers in multiple cortical and subcortical regions of PD using a proximity ligation assay (PLA). We observe widespread distribution of αSYN oligomers with PLA and more restricted distribution of LRP with αSYN immunohistochemistry. The distribution of αSYN oligomers differed from LRP in that αSYN oligomer burden was significantly greater in the neocortex, while LRP was greater in vulnerable subcortical regions, including the brainstem. We also found that cognitive impairment was associated with αSYN oligomers in the hippocampus. These results suggest that αSYN oligomers may be widely distributed in PD early in the disease process and that they may contribute to cognitive impairment in PD.
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