Treatment Combining Focused Ultrasound with Gastrodin Alleviates Memory Deficit and Neuropathology in an Alzheimer's Disease-Like Experimental Mouse Model. (13th January 2022)

• Record Type: Journal Article
• Authors: Luo, Kaixuan; Wang, Yuhong; Chen, Wen-Shiang; Feng, Xiangjun; Liao, Yehui; Chen, Shaochun; Liu, Yao; Liao, Chengde; Chen, Moxian; Ao, Lijuan
• Other Names: Lu Rongrong Academic Editor.
• Is Part Of: Neural plasticity. Volume 2022(2022)
• Publication Date: 2022-01-13
• Subjects: Neuroplasticity -- Periodicals; 612.82
• DOI: 10.1155/2022/5241449
• Languages: English
• ISSNs: 2090-5904

Abstract

Abstract : Alzheimer's disease (AD) is the most common type of dementia but lacks effective treatment at present. Gastrodin (GAS) is a phenolic glycoside extracted from the traditional Chinese herb—Gastrodia elata—and has been reported as a potential therapeutic agent for AD. However, its efficiency is reduced for AD patients due to its limited BBB permeability. Studies have demonstrated the feasibility of opening the blood-brain barrier (BBB) via focused ultrasound (FUS) to overcome the obstacles preventing medicines from blood flow into the brain tissue. We explored the therapeutic potential of FUS-mediated BBB opening combined with GAS in an AD-like mouse model induced by unilateral intracerebroventricular (ICV) injection of A β 1-42 . Mice were divided into 5 groups: control, untreated, GAS, FUS and FUS+GAS. Combined treatment (FUS+GAS) rather than single intervention (GAS or FUS) alleviated memory deficit and neuropathology of AD-like mice. The time that mice spent in the novel arm was prolonged in the Y-maze test after 15-day intervention, and the waste-cleaning effect was remarkably increased. Contents of A β, tau, and P-tau in the observed (also the targeted) hippocampus were reduced. BDNF, synaptophysin (SYN), and PSD-95 were upregulated in the combined group. Overall, our results demonstrate that FUS-mediated BBB opening combined with GAS injection exerts the potential to alleviate memory deficit and neuropathology in the AD-like experimental mouse model, which may be a novel strategy for AD treatment.