Abstract
Bushen-Tiansui Formula (BTF) was empirically updated from a classical prescription named Kong-Sheng-Zhen-Zhong pill. It is based on the traditional Chinese medicine theory of the mutual relationship between the brain and the kidney and is intended to treat neurodegenerative diseases. This formulation has been used for several years to treat patients with Alzheimer's disease- (AD-) like symptoms in our clinical department. However, the medicinal ingredients and the mechanisms by which BTF improves cognition and memory functions have not been characterized. In this study, we used UPLC-MS to generate a chromatographic fingerprinting of BTF and identified five possible active ingredients, including stilbene glycoside; epimedin A1, B, and C; and icariin. We also showed that oral administration of BTF reversed the cognitive defects in an Aβ1–42 fibril-infused rat model of AD, protected synaptic ultrastructure in the CA1 region, and restored the expression of BDNF, synaptotagmin (Syt), and PSD95. These effects likely occurred through the BDNF-activated receptor tyrosine kinase B (TrkB)/Akt/CREB signaling pathway. Furthermore, BTF exhibited no short-term or chronic toxicity in rats. Together, these results provided a scientific support for the clinical use of BTF to improve learning and memory in patients with AD.
Highlights
Alzheimer’s disease (AD) is the leading cause of dementia worldwide, but the etiology and pathogenesis of this disease have not been characterized
Treatment with Bushen-Tiansui Formula (BTF) reversed Aβ1–42 fibril-induced reduction of synaptic marker expression (Figure 3(h)). These results indicated that oral administration of BTF inhibited synaptic loss and improved synaptic plasticity in Aβ1–42 fibril-infused rats
Bushen-Tiansui Formula is an empirically improved version of the Kong-Sheng-ZhenZhon pill developed in our department by adjusting the composition and proportion of herbs, and the development of the application of BTF in neurological disorders was based on the theory of the kidney-brain axis
Summary
Alzheimer’s disease (AD) is the leading cause of dementia worldwide, but the etiology and pathogenesis of this disease have not been characterized. Over the last decade, a series of new drugs designed to clear neurofibrillary tangles have failed to improve or reverse AD, which indicated that neurofibrillary tangles correlated weakly with the degree of dementia in patients with AD [2]. Neurotrophins are growth factors that regulate neuronal development, differentiation, and survival. Brain-derived neurotrophic factor (BDNF) is an important neurotrophin that is distributed extensively throughout the central nervous system. Synaptotagmin and PSD95 confer protection by regulating the repair of synapses and the reconstruction of neural circuits to improve learning and memory in animals with dementia [4,5,6]. Studies have shown that the expression of BDNF was reduced in the brains of patients with AD with synaptic loss [7]. The outcomes of several clinical trials involved the intrathecal infusion of recombinant BDNF to treat patients with amyotrophic lateral sclerosis have been disappointing due to the short
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