中国神经再生研究(英文版) ›› 2025, Vol. 20 ›› Issue (12): 3525-3526.doi: 10.4103/NRR.NRR-D-24-00936

• 观点:退行性病与再生 • 上一篇    下一篇

跑步机运动能否有助于保持无斑块的健康大脑?

  

  • 出版日期:2025-12-15 发布日期:2025-03-15

Is it possible to maintain a plaquefree healthy brain by treadmill?

Swarupa Pahan, Kalipada Pahan*   

  1. Division of Research and Development, Jesse Brown Veterans Affairs Medical Center, Chicago, IL, USA (Pahan S, Pahan K) Department of Neurological Sciences, Rush University Medical Center, Chicago, IL, USA (Pahan K)
  • Online:2025-12-15 Published:2025-03-15
  • Contact: Kalipada Pahan, PhD, Kalipada_Pahan@rush.edu.
  • Supported by:
    This work was supported by merit awards (1I01BX005002 and I01BX005613) from US Department of Veterans Affairs and a grant (AT10980) from NIH (to KP). Moreover, Dr. Kalipada Pahan is the recipient of a Research Career Scientist Award (1IK6 BX004982) from the Department of Veterans Affairs. However, the views expressed in this article are those of the authors and do not necessarily reflect the position or policy of the Department of Veterans Affairs or the United States government.

摘要: https://orcid.org/0000-0001-6048-9598 (Kalipada Pahan)

Abstract: It is believed that overproduction and deposition of amyloid-β (Aβ) plaques in the hippocampus and cortex region of the brain cause neuronal dysfunction leading to cognitive impairments in Alzheimer’s disease (AD). Until now, there has been no effective treatment to reduce plaque load from the brain. Recent studies have shown that regular treadmill exercise lowers plaques from the brain of a mouse model of AD. Out of three proteolytic enzymes or secretases, while α-secretase activates the non-amyloidogenic pathway of amyloid precursor protein (APP) cleavage to inhibit Aβ plaque production, β- and γ-secretases indulge the APP cleavage in the amyloidogenic pathway for the formation of Aβ plaques. Accordingly, it is nice to see that treadmill run increases α-secretase and decreases β- and γ-secretases in AD mice. Interestingly, in normalaged mice as well, a treadmill run increases α-secretase and decreases β- and γ-secretases, indicating that in normal subjects as well, a treadmill run may keep the formation of Aβ plaques at bay. The prototype role of peroxisome proliferator-activated receptor α (PPARα), a nuclear hormone receptor, is to regulate energy homeostasis via catabolism of fatty acids. However, it has been shown that the success of treadmill run depends on PPARα as the treadmill remains ineffective in increasing α-secretase and reducing plaque burden in AD mice lacking PPARα. Here, we discuss about this drug-free safe approach and associated PPARα-dependent mechanisms for the inhibition of plaque pathogenesis.