1. Academic Validation
  2. Berberine Rescues D-Ribose-Induced Alzheimer's Pathology via Promoting Mitophagy

Berberine Rescues D-Ribose-Induced Alzheimer's Pathology via Promoting Mitophagy

  • Int J Mol Sci. 2023 Mar 20;24(6):5896. doi: 10.3390/ijms24065896.
Chuanling Wang 1 Qian Zou 2 3 Yinshuang Pu 2 3 Zhiyou Cai 2 3 Yong Tang 1
Affiliations

Affiliations

  • 1 Department of Histology and Embryology, School of Basic Medicine, Chongqing Medical University, No. 1 Yixueyuan Road, Yuzhong District, Chongqing 400016, China.
  • 2 Chongqing Key Laboratory of Neurodegenerative Diseases, No. 118 Xingguang Avenue, Liangjiang New Area, Chongqing 401147, China.
  • 3 Department of Neurology, Chongqing General Hospital, No. 118 Xingguang Avenue, Liangjiang New Area, Chongqing 401147, China.
Abstract

Mitochondrial dysfunction is considered an early event of Alzheimer disease (AD). D-ribose is a natural monosaccharide that exists in cells, especially in mitochondria, and can lead to cognitive dysfunction. However, the reason for this is unclear. Berberine (BBR) is an isoquinoline alkaloid that can target mitochondria and has great prospect in the treatment of AD. The methylation of PINK1 reinforces the burden of Alzheimer's pathology. This study explores the role of BBR and D-ribose in the Mitophagy and cognitive function of AD related to DNA methylation. APP/PS1 mice and N2a cells were treated with D-ribose, BBR, and Mitophagy inhibitor Mdivi-1 to observe their effects on mitochondrial morphology, Mitophagy, neuron histology, AD pathology, animal behavior, and PINK1 methylation. The results showed that D-ribose induced mitochondrial dysfunction, Mitophagy damage, and cognitive impairment. However, BBR inhibition of PINK1 promoter methylation can reverse the above effects caused by D-ribose, improve mitochondrial function, and restore Mitophagy through the PINK1-Parkin pathway, thus reducing cognitive deficits and the burden of AD pathology. This experiment puts a new LIGHT on the mechanism of action of D-ribose in cognitive impairment and reveals new insights in the use of BBR for AD treatment.

Keywords

Alzheimer’s disease; BBR; D-ribose; cognition; mitophagy.

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