中国神经再生研究(英文版) ›› 2021, Vol. 16 ›› Issue (8): 1467-1482.doi: 10.4103/1673-5374.303007

• 综述:退行性病与再生 • 上一篇    下一篇

调节神经元生物能是治疗神经退行性疾病的潜在策略

  

  • 出版日期:2021-08-15 发布日期:2021-01-13

Regulation of neuronal bioenergetics as a therapeutic strategy in neurodegenerative diseases

Isaac G. Onyango1, *, James P. Bennett, Jr2, Gorazd B. Stokin1   

  1. 1Center for Translational Medicine, International Clinical Research Centre (ICRC), St. Anne’s University Hospital, Brno, Czech Republic; 2Neurodegeneration Therapeutics, 3050A Berkmar Drive, Charlottesville, VA, USA
  • Online:2021-08-15 Published:2021-01-13
  • Contact: Isaac G. Onyango, DVM, PhD, isaac.onyango@fnusa.cz.
  • Supported by:
    This work was supported by the European Regional Development Fund - Project MAGNET (No. CZ.02.1.01/0.0/0.0/15_003/0000492).

摘要: https://orcid.org/0000-0003-1650-1937 (Isaac G. Onyango) 

Abstract: Neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis are a heterogeneous group of debilitating disorders with multifactorial etiologies and pathogeneses that manifest distinct molecular mechanisms and clinical manifestations with abnormal protein dynamics and impaired bioenergetics. Mitochondrial dysfunction is emerging as an important feature in the etiopathogenesis of these age-related neurodegenerative diseases. The prevalence and incidence of these diseases is on the rise with the increasing global population and average lifespan. Although many therapeutic approaches have been tested, there are currently no effective treatment routes for the prevention or cure of these diseases. We present the current status of our knowledge and understanding of the involvement of mitochondrial dysfunction in these diseases and highlight recent advances in novel therapeutic strategies targeting neuronal bioenergetics as potential approach for treating these diseases.

Key words: aging, Alzheimer’s disease, amyotrophic lateral sclerosis, Huntington’s disease, mitochondrial biogenesis, mitochondrial dysfunction, mtDNA mutations, neurodegeneration, oxidative stress, Parkinson’s disease