ArticleNPJ Parkinson's disease2022
Reduced synaptic activity and dysregulated extracellular matrix pathways in midbrain neurons from Parkinson's disease patients.
Article in NPJ Parkinson's disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Proteins and Transcriptional Dysregulation of the Brain Extracellular Matrix in Parkinson's Disease: A Systematic Review.International journal of molecular sciences · 2023Pooled it
- Disulfidptosis contributes to rotenone-induced dopaminergic neuron damage.Neural regeneration research · 2026Article
- Dysregulation of the Extracellular Matrix in the Synaptic Pathology of Parkinson's Disease: Molecular Mechanisms and Novel Therapeutic Approaches.Life (Basel, Switzerland) · 2026Review
- The Emerging Parkinson's Disease Oxylipin-Ome.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- The extracellular matrix as a dynamic regulator of brain function and plasticity.Neurobiology of disease · 2026Review
- The epitranscriptomic m6A RNA modification modulates the synapse in ageing and in a mouse model of synucleinopathy.NPJ Parkinson's disease · 2026Article
- Review
- Disruption of Synaptic Vesicle Trafficking in Alzheimer's and Parkinson's Disease: Mechanisms and Therapeutic Implication.International journal of molecular sciences · 2026Review
- New insights into synaptic vesicle dysfunction in Parkinson's disease.Journal of Parkinson's disease · 2026Review
- Extracellular vesicles from stem cells rescue cellular phenotypes and behavioral deficits in SHANK3-associated ASD neuronal and mouse models.Cell death & disease · 2026Article
- SNCA triplication disrupts proteostasis and extracellular architecture prior to neurodegeneration in human midbrain organoids.NPJ Parkinson's disease · 2026Article
- Optogenetic-induced α-synuclein accumulation reveals early synaptic dysfunction in experimental models of Parkinson's disease.NPJ Parkinson's disease · 2025Article
- Volumetric spline-based Kolmogorov-Arnold architectures surpass CNNs, vision transformers, and graph networks for Parkinson's disease detection.Communications medicine · 2025Article
- Sleep deprivation and risk for Parkinson's disease: evidence and therapeutic implications.Journal of neurology · 2025Review
- A Transcriptomic Roadmap of Parkinson's Disease Progression at Single Cell Resolution.medRxiv : the preprint server for health sciences · 2025Article
- Formation of seeding-competent α-synuclein aggregates in parkin-deficient iPSC-derived human neurons.NPJ Parkinson's disease · 2025Article
- A hypothesis explaining Alzheimer's disease, Parkinson's disease, and dementia with Lewy bodies overlap.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Degenerative Disease Diagnosis and Analysis Based on Tissue Specificity of DNA Methylation.International journal of molecular sciences · 2025Article
- Park7 deletion leads to sex-specific transcriptome changes involving NRF2-CYP1B1 axis in mouse midbrain astrocytes.NPJ Parkinson's disease · 2025Article
- Substantia nigra and blood gene signatures and biomarkers for Parkinson's disease from integrated multicenter microarray-based transcriptomic analyses.Frontiers in aging neuroscience · 2025Article
Corrections and comments
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Authors and funding
33 authors at 8 institutions in 6 countries.
Funding
Abstract
Several mutations that cause Parkinson's disease (PD) have been identified over the past decade. These account for 15-25% of PD cases; the rest of the cases are considered sporadic. Currently, it is accepted that PD is not a single monolithic disease but rather a constellation of diseases with some common phenotypes. While rodent models exist for some of the PD-causing mutations, research on the sporadic forms of PD is lagging due to a lack of cellular models. In our study, we differentiated PD patient-derived dopaminergic (DA) neurons from the induced pluripotent stem cells (iPSCs) of several PD-causing mutations as well as from sporadic PD patients. Strikingly, we observed a common neurophysiological phenotype: neurons derived from PD patients had a severe reduction in the rate of synaptic currents compared to those derived from healthy controls. While the relationship between mutations in genes such as the SNCA and LRRK2 and a reduction in synaptic transmission has been investigated before, here we show evidence that the pathogenesis of the synapses in neurons is a general phenotype in PD. Analysis of RNA sequencing results displayed changes in gene expression in different synaptic mechanisms as well as other affected pathways such as extracellular matrix-related pathways. Some of these dysregulated pathways are common to all PD patients (monogenic or idiopathic). Our data, therefore, show changes that are central and convergent to PD and suggest a strong involvement of the tetra-partite synapse in PD pathophysiology.
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Registered trials
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