ArticleFrontiers in neuroinformatics2020
A Multi-Scale Computational Model of Excitotoxic Loss of Dopaminergic Cells in Parkinson's Disease.
Article in Frontiers in neuroinformatics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 11 citations in OpenAlex.
- Dysfunctional LHX6 pallido-subthalamic projections mediate epileptic events in a mouse model of Leigh syndrome.The Journal of clinical investigation · 2025Article
- Multiple time delay induced Hopf bifurcation of a cortex - basal ganglia model for Parkinson's Disease.Cognitive neurodynamics · 2024Article
- Azilsartan improves doxorubicin-induced cardiotoxicity via inhibiting oxidative stress, proinflammatory pathway, and apoptosis.Journal of medicine and life · 2023Article
- A Multi-Scale Computational Model of Levodopa-Induced Toxicity in Parkinson's Disease.Frontiers in neuroscience · 2022Article
- DOPA Homeostasis by Dopamine: A Control-Theoretic View.International journal of molecular sciences · 2021Article
- Influence of energy deficiency on the subcellular processes of Substantia Nigra Pars Compacta cell for understanding Parkinsonian neurodegeneration.Scientific reports · 2021Article
- A Multiscale, Systems-Level, Neuropharmacological Model of Cortico-Basal Ganglia System for Arm Reaching Under Normal, Parkinsonian, and Levodopa Medication Conditions.Frontiers in computational neuroscience · 2021Article
- A Multi-Scale Computational Model of Excitotoxic Loss of Dopaminergic Cells in Parkinson's Disease.Frontiers in neuroinformatics · 2020Article
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2 authors at 1 institution in 1 country.
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Abstract
Parkinson's disease (PD) is a neurodegenerative disorder caused by loss of dopaminergic neurons in substantia nigra pars compacta (SNc). Although the exact cause of cell death is not clear, the hypothesis that metabolic deficiency is a key factor has been gaining attention in recent years. In the present study, we investigated this hypothesis using a multi-scale computational model of the subsystem of the basal ganglia comprising the subthalamic nucleus (STN), globus pallidus externa (GPe), and SNc. The proposed model is a multiscale model in that interaction among the three nuclei are simulated using more abstract Izhikevich neuron models, while the molecular pathways involved in cell death of SNc neurons are simulated in terms of detailed chemical kinetics. Simulation results obtained from the proposed model showed that energy deficiencies occurring at cellular and network levels could precipitate the excitotoxic loss of SNc neurons in PD. At the subcellular level, the models show how calcium elevation leads to apoptosis of SNc neurons. The therapeutic effects of several neuroprotective interventions are also simulated in the model. From neuroprotective studies, it was clear that glutamate inhibition and apoptotic signal blocker therapies were able to halt the progression of SNc cell loss when compared to other therapeutic interventions, which only slowed down the progression of SNc cell loss.
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