ArticleNature communications2024
Site-specific seeding of Lewy pathology induces distinct pre-motor cellular and dendritic vulnerabilities in the cortex.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Gray Matter Microstructure Measured Using Diffusion Imaging as a Biomarker of Severity in Lewy Body Diseases.Movement disorders : official journal of the Movement Disorder Society · 2026Article
- Blood-catalyzed n-doped polymers for reversible optical neural control.Science (New York, N.Y.) · 2026Article
- Cortical and basal ganglia beta oscillations and frequency-dependent DBS effects in the A53T Parkinson's disease rat model.NPJ Parkinson's disease · 2026Article
- Alpha-Synuclein in Neurodegeneration: From Shared Biology to Disease-Specific Phenotypes.Cells · 2026Review
- Characterization of motor and non-motor features associated with bilateral nigral degeneration due to A53T alpha-synuclein in female rats.Scientific reports · 2026Article
- Functional Magnetic Resonance Imaging (fMRI) Signatures of Progression and Phenoconversion in Prodromal Synucleinopathies.Movement disorders : official journal of the Movement Disorder Society · 2025Article
- Cortical α-synuclein pathology induces cell autonomous neuronal hypoactivity and compensatory circuit changes in a model of early Lewy body dementia.bioRxiv : the preprint server for biology · 2025Article
- Phosphoproteome modifications and cortical circuit dysfunction are linked to the early-stage progression of alpha-synuclein aggregation.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Circuit-based biomarkers distinguishing the gradual progression of Lewy pathology across synucleinopathies remain unknown. Here, we show that seeding of α-synuclein preformed fibrils in mouse dorsal striatum and motor cortex leads to distinct prodromal-phase cortical dysfunction across months. Our findings reveal that while both seeding sites had increased cortical pathology and hyperexcitability, distinct differences in electrophysiological and cellular ensemble patterns were crucial in distinguishing pathology spread between the two seeding sites. Notably, while beta-band spike-field-coherence reflected a significant increase beginning in Layer-5 and then spreading to Layer-2/3, the rate of entrainment and the propensity of stochastic beta-burst dynamics was markedly seeding location-specific. This beta dysfunction was accompanied by gradual superficial excitatory ensemble instability following cortical, but not striatal, preformed fibrils injection. We reveal a link between Layer-5 dendritic vulnerabilities and translaminar beta event dysfunction, which could be used to differentiate symptomatically similar synucleinopathies.
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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 Socratic graph.