中国神经再生研究(英文版) ›› 2024, Vol. 19 ›› Issue (9): 1879-1880.doi: 10.4103/1673-5374.391187

• 观点:退行性病与再生 • 上一篇    下一篇

用于神经退行性变解码的非线性动态状态空间网络建模

  

  • 出版日期:2024-09-15 发布日期:2024-01-25

Non-linear dynamic state-space network modeling for decoding neurodegeneration

Venkata C. Chirumamilla, Chi Wang Ip, Martin Reich, Robert Peach, Jens Volkmann, Bahman Nasseroleslami, Muthuraman Muthuraman*   

  1. Prenatal Pediatrics Institute, Children’s National Hospital, Washington, DC, USA (Chirumamilla VC)
    Neural Engineering with Signal Analytics and Artificial Intelligence, Department of Neurology, University of Würzburg, Würzburg, Germany (Ip CW, Reich M, Peach R, Volkmann J, Muthuraman M) 
    Academic Unit of Neurology, Trinity Biomedical Sciences Institute, Trinity College Dublin, University of Dublin, Dublin, Ireland (Nasseroleslami B)
  • Online:2024-09-15 Published:2024-01-25
  • Contact: Muthuraman Muthuraman, PhD, muthuraman_m@ukw.de.
  • Supported by:
    This work was supported by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) Project-ID 424778381-TRR 295 and the Fondazione Grigioni per il Morbo di Parkinson (to MM).

摘要: https://orcid.org/0000-0001-6158-2663 (Muthuraman Muthuraman)

Abstract: Neurodegenerative disorders represent a pervasive global health challenge, yet therapeutic options remain conspicuously limited. These disorders are inherently dynamic processes within the central nervous system, unfolding across distinct sub-stages: initial structural neuronal alterations (sub-stage 1), functional impairment (sub-stage 2), and culminating in neuronal death (sub-stage 3). Previous studies have revealed shared pathological features between amyotrophic lateral sclerosis (ALS) and Parkinson’s disease (PD) (van Rheenen et al., 2021; Mantle and Hargreaves, 2022) including common genetic risk factors identified through genome-wide association studies (van Rheenen et al., 2021). Both disorders manifest similar neurodegenerative mechanisms, such as oligomer formation, aberrant protein accumulation, and protein misfolding-specifically, superoxide dismutase 1 in ALS and α-synuclein in PD. Mitochondrial dysfunction further serves as a common denominator in the pathogenesis of ALS and PD (Mantle and Hargreaves, 2022).