ArticleScientific reports2017
Subthalamic Nucleus Deep Brain Stimulation Does Not Modify the Functional Deficits or Axonopathy Induced by Nigrostriatal α-Synuclein Overexpression.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Systematic review of rodent studies of deep brain stimulation for the treatment of neurological, developmental and neuropsychiatric disorders.Translational psychiatry · 2024Pooled it
- Optogenetic regulation of chloride ions in reactive astrocytes may mitigate Parkinson's disease pathology.Scientific reports · 2025Article
- Standardized wireless deep brain stimulation system for mice.NPJ Parkinson's disease · 2024Article
- High frequency electrical stimulation reduces α-synuclein levels and α-synuclein-mediated autophagy dysfunction.Scientific reports · 2024Article
- Subthalamic nucleus but not entopeduncular nucleus deep brain stimulation enhances neurogenesis in the SVZ-olfactory bulb system of Parkinsonian rats.Frontiers in cellular neuroscience · 2024Article
- Effect of deep brain stimulation compared with drug therapy alone on the progression of Parkinson's disease.Frontiers in neuroscience · 2023Article
- Neuroprotection and Non-Invasive Brain Stimulation: Facts or Fiction?International journal of molecular sciences · 2022Review
- Surgical Management of Synucleinopathies.Biomedicines · 2022Article
- How Does Deep Brain Stimulation Change the Course of Parkinson's Disease?Movement disorders : official journal of the Movement Disorder Society · 2022Review
- Post-mortem brain histological examination in the substantia nigra and subthalamic nucleus in Parkinson's disease following deep brain stimulation.Frontiers in neuroscience · 2022Article
- Striatal Afferent BDNF Is Disrupted by Synucleinopathy and Partially Restored by STN DBS.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Cylinder Test to Assess Sensory-motor Function in a Mouse Model of Parkinson's Disease.Bio-protocol · 2019Article
- Emerging therapies in Parkinson disease - repurposed drugs and new approaches.Nature reviews. Neurology · 2019Review
- Deep brain stimulation: potential for neuroprotection.Annals of clinical and translational neurology · 2019Review
- BDNF provides many routes toward STN DBS-mediated disease modification.Movement disorders : official journal of the Movement Disorder Society · 2019Article
- Quality Over Quantity: Advantages of Using Alpha-Synuclein Preformed Fibril Triggered Synucleinopathy to Model Idiopathic Parkinson's Disease.Frontiers in neuroscience · 2018Article
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12 authors at 3 institutions in 1 country.
Funding
Abstract
Subthalamic nucleus deep brain stimulation (STN DBS) protects dopaminergic neurons of the substantia nigra pars compacta (SNpc) against 6-OHDA and MPTP. We evaluated STN DBS in a parkinsonian model that displays α-synuclein pathology using unilateral, intranigral injections of recombinant adeno-associated virus pseudotype 2/5 to overexpress wildtype human α-synuclein (rAAV2/5 α-syn). A low titer of rAAV2/5 α-syn results in progressive forelimb asymmetry, loss of striatal dopaminergic terminal density and modest loss of SNpc dopamine neurons after eight weeks, corresponding to robust human-Snca expression and no effect on rat-Snca, Th, Bdnf or Trk2. α-syn overexpression increased phosphorylation of ribosomal protein S6 (p-rpS6) in SNpc neurons, a readout of trkB activation. Rats received intranigral injections of rAAV2/5 α-syn and three weeks later received four weeks of STN DBS or electrode implantation that remained inactive. STN DBS did not protect against α-syn-mediated deficits in forelimb akinesia, striatal denervation or loss of SNpc neuron, nor did STN DBS elevate p-rpS6 levels further. ON stimulation, forelimb asymmetry was exacerbated, indicating α-syn overexpression-mediated neurotransmission deficits. These results demonstrate that STN DBS does not protect the nigrostriatal system against α-syn overexpression-mediated toxicity. Whether STN DBS can be protective in other models of synucleinopathy is unknown.
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