中国神经再生研究(英文版) ›› 2025, Vol. 20 ›› Issue (3): 794-796.doi: 10.4103/NRR.NRR-D-23-02106

• 观点:退行性病与再生 • 上一篇    下一篇

神经退行性疾病和衰老的线粒体治疗和线粒体转移

  

  • 出版日期:2025-03-15 发布日期:2024-06-26

Mitochondrial therapeutics and mitochondrial transfer for neurodegenerative diseases and aging

Neville Ng*, #, Michelle Newbery#, Nicole Miles, Lezanne Ooi*   

  1. Molecular Horizons and School of Chemistry and Molecular Bioscience, University of Wollongong, Wollongong, NSW, Australia
  • Online:2025-03-15 Published:2024-06-26
  • Contact: Lezanne Ooi, PhD,lezanne@uow.edu.au; Neville Ng, PhD,nevillen@uow.edu.au.
  • Supported by:
    This work was supported by a MAWA Project Grant (to NN, MN, LO). The aim of MAWA is to advance medical science and improve human health and therapeutic interventions without the use of animals or animal products.

摘要:

https://orcid.org/0000-0001-9241-8268 (Lezanne Ooi) 

https://orcid.org/0000-0003-1478-9850 (Neville Ng)

Abstract: Mitochondrial dysfunction and neurodegeneration: Progressive neurodegenerative diseases affect a significant proportion of the population; in a single year, there are as many as 276 million disabilities and 9 million deaths as a result of neurological diseases. Mitochondrial function, aging, and neurodegenerative processes appear to be intricately linked; central nervous system degeneration is a major feature of loss-of-function mitochondrial diseases, involving mutation of nuclear or mitochondrial DNA. Meanwhile, mitochondrial dysfunction occurs during healthy aging and is further associated with several neurological diseases, including Alzheimer’s disease (AD), Huntington’s disease, Friedreich’s ataxia, multiple sclerosis, motor neuron disease, Parkinson’s disease (PD), and vanishing white matter disease (VWMD) (Figure 1A). Aging increases neurodegenerative risk factors and processes, including progressively impaired cognitive and/or motor function due to cellular dysfunction, senescence, and/or neuronal death. Furthermore, impaired mitochondrial respiration, biogenesis, mitophagy, and axonal transport can be causative factors in dysfunctional protein synthesis, folding, aggregation, and trafficking, as well as inflammation, oxidative stress, and genomic instability.