Da-Bu-Yin-Wan rescues cognitive deficits in aging and Alzheimer's disease models by Wnt/β-catenin-dependent restoration of lysosomal acidification.

Haijun Zhang, Hao Zhang, Meihuan Zhao, Wenjun Luo, Simin Chen, Ping Wang, Xiao Liu, Shijun Xu

State Key Laboratory of Southwestern Chinese Medicine Resources, Chengdu University of Traditional Chinese Medicine, Chengdu, China; School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China; Institute of Material Medica Integration and Transformation for Brain Disorders, Chengdu University of Traditional Chinese Medicine, Chengdu, China.State Key Laboratory of Southwestern Chinese Medicine Resources, Chengdu University of Traditional Chinese Medicine, Chengdu, China; School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China; Institute of Material Medica Integration and Transformation for Brain Disorders, Chengdu University of Traditional Chinese Medicine, Chengdu, China. · pubmed

Paper

Abstract

Lysosomal acidification deficits are increasingly recognized as a convergent pathological mechanism driving both age-related cognitive decline (ARCD) and early Alzheimer's disease (AD) progression, creating a self-reinforcing cycle of cellular aging and Aβ dyshomeostasis. Despite demonstrated neuroprotective effects of Da-Bu-Yin-Wan (DBYW) in Parkinson's disease models, its therapeutic potential for lysosomal dysfunction in ARCD and AD remains an uncharted area of investigation.

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Research summary

Da-Bu-Yin-Wan improves cognitive deficits in aging and Alzheimer's disease models by restoring lysosomal acidification through Wnt/β-catenin signaling. The paper addresses a potential therapeutic approach to a root cause of cognitive decline associated with aging and Alzheimer's disease, focusing on lysosomal dysfunction, which is relevant to longevity research.

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