中国神经再生研究(英文版) ›› 2026, Vol. 21 ›› Issue (1): 306-307.doi: 10.4103/NRR.NRR-D-24-01034

• 观点:退行性病与再生 • 上一篇    下一篇

有氧运动诱导肌动蛋白鸢尾素释放:促进神经保护和改善认知功能的新策略

  

  • 出版日期:2026-01-15 发布日期:2025-04-23

Aerobic exercise–induced myokine irisin release: A novel strategy to promote neuroprotection and improve cognitive function

Jae-Won Choi, Rengasamy Balakrishnan*   

  1. Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, FL, USA Department of Applied Life Science, Graduate School, Konkuk University, Chungju, South Korea Department of Biotechnology, College of Biomedical and Health Science, Research Institute of Inflammatory Disease (RID), Konkuk University, Chungju, South Korea
  • Online:2026-01-15 Published:2025-04-23
  • Contact: Rengasamy Balakrishnan, PhD, balakonkuk@kku.ac.kr.
  • Supported by:
    This work was supported by The Basic Science Research Program through the National Research Foundation of Korea (NRF), funded by the Ministry of Education (RS2023-00244901) (to RB).

摘要: https://orcid.org/0000-0001-8135-8183 (Rengasamy Balakrishnan)

Abstract: Challenges in the prevention and treatment of mild cognitive impairment associated with Alzheimer’s disease: Increased life expectancy due to advancements in medical care has given rise to an aging population, accompanied by a surge in the incidence of incurable neurodegenerative diseases (NDDs). These diseases primarily affect the cognitive and behavioral functions of older adults by impacting brain activity. Mild cognitive impairment (MCI) is a neurodegenerative condition that affects a significant portion of the population. Characterized by memory loss, MCI is believed to be an early indication of Alzheimer’s disease (AD) and is generally considered to be a transitional state between healthy aging and AD onset. Currently, 24 million people worldwide are affected by AD, a number projected to increase fourfold by 2050. By this date, the global population over 65 years is expected to be triple what it was in 2010, at nearly 1.5 billion individuals. While cognitive and behavioral impairment are the first clinical symptoms of AD, memory loss typically appears before clinical diagnosis—particularly in people over 65 years of age—due to progressive loss of neurons and synapses, mainly in the cortex and hippocampus. By the time, AD is clinically diagnosed, several pathological changes in the brain are already in progress, including oxidative stress, amyloid-β (Aβ) and tau protein accumulation, metabolism alterations, blood–brain barrier dysfunction, microbiotagut-brain axis dysfunction, mitochondrial dysfunction, and neuronal apoptosis. In pathological studies, excessive neuroinflammatory response and injury lead to the depletion of neurons in terms of structure, function, or quantity, resulting in the impairment of learning, memory, and other cognitive functions. These effects result in the early stages of MCI, which is associated with AD (Amartumur et al., 2024).