Parkinson’s disease rodent models: Are they suitable for DBS research?

Ruiz, Miguel Cesar Merino; Guimarães, Rayanne Poletti; Mortari, Márcia Renata

doi:10.1016/j.jneumeth.2022.109687

Cited by 4 publications

(2 citation statements)

References 133 publications

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“…Additionally, only short-term stimulation was delivered in the rodent experiment, whether a long-term stimulation could exert neuroprotection, and through a similar mechanism remains unknown. The previous study also addressed the limitation of rodents in the DBS study 31 . Therefore, we illustrated these issues and confirmed our findings, using the tissue from NHP and CSF from patients after long-term stimulation.…”

Section: Discussionmentioning

confidence: 99%

Subthalamic nucleus deep brain stimulation alleviates oxidative stress via mitophagy in Parkinson’s disease

Chen,

Zhu,

Yuan

et al. 2024

npj Parkinsons Dis.

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Subthalamic nucleus deep brain stimulation (STN-DBS) has the potential to delay Parkinson’s disease (PD) progression. Whether oxidative stress participates in the neuroprotective effects of DBS and related signaling pathways remains unknown. To address this, we applied STN-DBS to mice and monkey models of PD and collected brain tissue to evaluate mitophagy, oxidative stress, and related pathway. To confirm findings in animal experiments, a cohort of PD patients was recruited and oxidative stress was evaluated in cerebrospinal fluid. When PD mice received STN stimulation, the mTOR pathway was suppressed, accompanied by elevated LC3 II expression, increased mitophagosomes, and a decrease in p62 expression. The increase in mitophagy and balance of mitochondrial fission/fusion dynamics in the substantia nigra caused a marked enhancement of the antioxidant enzymes superoxide dismutase and glutathione levels. Subsequently, fewer mitochondrial apoptogenic factors were released to the cytoplasm, which resulted in a suppression of caspase activation and reservation of dopaminergic neurons. While interfaced with an mTOR activator, oxidative stress was no longer regulated by STN-DBS, with no neuroprotective effect. Similar results to those found in the rodent experiments were obtained in monkeys treated with chronic STN stimulation. Moreover, antioxidant enzymes in PD patients were increased after the operation, however, there was no relation between changes in antioxidant enzymes and motor impairment. Collectively, our study found that STN-DBS was able to increase mitophagy via an mTOR-dependent pathway, and oxidative stress was suppressed due to removal of damaged mitochondria, which was attributed to the dopaminergic neuroprotection of STN-DBS in PD.

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Section: Discussionmentioning

confidence: 99%

Subthalamic nucleus deep brain stimulation alleviates oxidative stress via mitophagy in Parkinson’s disease

Chen,

Zhu,

Yuan

et al. 2024

npj Parkinsons Dis.

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“…The 6‐hydroxydopamine (6‐OHDA) lesioned rodent models are extensively employed in basic research due to their resemblance to PD patients 15 . They display augmented daytime activity and more nocturnal sleep episodes during the night, resembling the characteristic features of nocturnal insomnia and daytime sleepiness, which are commonly observed in PD patients 2 .…”

Section: Introductionmentioning

confidence: 99%

Automatic sleep–wake classification and Parkinson's disease recognition using multifeature fusion with support vector machine

Shen,

Huai,

Wang

et al. 2024

CNS Neurosci Ther

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AimsSleep disturbance is a prevalent nonmotor symptom of Parkinson's disease (PD), however, assessing sleep conditions is always time‐consuming and labor‐intensive. In this study, we performed an automatic sleep–wake state classification and early diagnosis of PD by analyzing the electrocorticography (ECoG) and electromyogram (EMG) signals of both normal and PD rats.MethodsThe study utilized ECoG power, EMG amplitude, and corticomuscular coherence values extracted from normal and PD rats to construct sleep–wake scoring models based on the support vector machine algorithm. Subsequently, we incorporated feature values that could act as diagnostic markers for PD and then retrained the models, which could encompass the identification of vigilance states and the diagnosis of PD.ResultsFeatures extracted from occipital ECoG signals were more suitable for constructing sleep–wake scoring models than those from frontal ECoG (average Cohen's kappa: 0.73 vs. 0.71). Additionally, after retraining, the new models demonstrated increased sensitivity to PD and accurately determined the sleep–wake states of rats (average Cohen's kappa: 0.79).ConclusionThis study accomplished the precise detection of substantia nigra lesions and the monitoring of sleep–wake states. The integration of circadian rhythm monitoring and disease state assessment has the potential to improve the efficacy of therapeutic strategies considerably.

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