ArticleBrain : a journal of neurology2017
Synaptic phosphorylated α-synuclein in dementia with Lewy bodies.
Article in Brain : a journal of neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 123 citations in OpenAlex.
- VGF Peptides in Cerebrospinal Fluid of Patients with Dementia with Lewy Bodies.International journal of molecular sciences · 2019Trial
- Review
- Imbalance in excitation and inhibition in sgACC is associated with depression in dementia with Lewy bodies.Translational psychiatry · 2026Article
- DYRK1A and Parkinson's disease, facts and hypotheses.Neurobiology of disease · 2026Review
- Role of α-Synuclein in the Prefrontal Cortex: From Physiological Synaptic Modulation to Synaptic Failure in Parkinson's Disease.Biomedicines · 2026Review
- Lewy Bodies Are Not Associated With Neuronal or Synaptic Loss in Dementia With Lewy Bodies.Neuropathology and applied neurobiology · 2026Article
- Seven tesla MRI reveals amygdala and hippocampal subfield atrophy in dementia with Lewy bodies.Alzheimer's research & therapy · 2026Article
- Imaging spatial transcriptomics reveals molecular patterns underlying accumulation of p-Ser129 α-synuclein in a transgenic mouse model.NPJ Parkinson's disease · 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
- Optogenetic-induced α-synuclein accumulation reveals early synaptic dysfunction in experimental models of Parkinson's disease.NPJ Parkinson's disease · 2025Article
- Synaptic enrichment of pSer129 alpha-synuclein correlates with dopaminergic denervation in early-stage Parkinson's disease.Nature communications · 2025Article
- Synapse vulnerability and resilience across the clinical spectrum of dementias.Nature reviews. Neurology · 2025Review
- Formation of seeding-competent α-synuclein aggregates in parkin-deficient iPSC-derived human neurons.NPJ Parkinson's disease · 2025Article
- Early α-synuclein aggregation decreases corticostriatal glutamate drive and synapse density.Neurobiology of disease · 2025Article
- A case of dementia with Lewy bodies with psychosis induced by low-dose gabapentinoids.BMC psychiatry · 2025Article
- Accumulation of alpha-synuclein pathology in the liver exhibits post-translational modifications associated with Parkinson's disease.iScience · 2024Article
- MJF-14 proximity ligation assay detects early non-inclusion alpha-synuclein pathology with enhanced specificity and sensitivity.NPJ Parkinson's disease · 2024Article
- Excitatory synaptic structural abnormalities produced by templated aggregation of α-syn in the basolateral amygdala.Neurobiology of disease · 2024Article
- Enhanced Spine Stability and Survival Lead to Increases in Dendritic Spine Density as an Early Response to Local Alpha-Synuclein Overexpression in Mouse Prefrontal Cortex.Cellular and molecular neurobiology · 2024Article
- Integration of iPSC-Derived Microglia into Brain Organoids for Neurological Research.International journal of molecular sciences · 2024Review
19 more citing papers are in PubMed but not listed here.
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23 authors at 9 institutions in 3 countries.
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Abstract
Dementia with Lewy bodies is characterized by the accumulation of Lewy bodies and Lewy neurites in the CNS, both of which are composed mainly of aggregated α-synuclein phosphorylated at Ser129. Although phosphorylated α-synuclein is believed to exert toxic effects at the synapse in dementia with Lewy bodies and other α-synucleinopathies, direct evidence for the precise synaptic localization has been difficult to achieve due to the lack of adequate optical microscopic resolution to study human synapses. In the present study we applied array tomography, a microscopy technique that combines ultrathin sectioning of tissue with immunofluorescence allowing precise identification of small structures, to quantitatively investigate the synaptic phosphorylated α-synuclein pathology in dementia with Lewy bodies. We performed array tomography on human brain samples from five patients with dementia with Lewy bodies, five patients with Alzheimer's disease and five healthy control subjects to analyse the presence of phosphorylated α-synuclein immunoreactivity at the synapse and their relationship with synapse size. Main analyses were performed in blocks from cingulate cortex and confirmed in blocks from the striatum of cases with dementia with Lewy bodies. A total of 1 318 700 single pre- or postsynaptic terminals were analysed. We found that phosphorylated α-synuclein is present exclusively in dementia with Lewy bodies cases, where it can be identified in the form of Lewy bodies, Lewy neurites and small aggregates (<0.16 µm3). Between 19% and 25% of phosphorylated α-synuclein deposits were found in presynaptic terminals mainly in the form of small aggregates. Synaptic terminals that co-localized with small aggregates of phosphorylated α-synuclein were significantly larger than those that did not. Finally, a gradient of phosphorylated α-synuclein aggregation in synapses (pre > pre + post > postsynaptic) was observed. These results indicate that phosphorylated α-synuclein is found at the presynaptic terminals of dementia with Lewy bodies cases mainly in the form of small phosphorylated α-synuclein aggregates that are associated with changes in synaptic morphology. Overall, our data support the notion that pathological phosphorylated α-synuclein may disrupt the structure and function of the synapse in dementia with Lewy bodies.
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