Intermittent Theta Burst Stimulation Attenuates Cognitive Deficits and Alzheimer’s Disease-Type Pathologies via ISCA1-Mediated Mitochondrial Modulation in APP/PS1 Mice
作者机构：Department of Rehabilitation MedicineDaping HospitalArmy Medical UniversityChongqing 400042China Department of Neurology and Center for Clinical NeuroscienceDaping HospitalArmy Medical UniversityChongqing 400042China Department of Special MedicineDaping HospitalArmy Medical UniversityChongqing 400042China
出 版 物：《Neuroscience Bulletin》 (神经科学通报（英文版）)
年 卷 期：2024年第40卷第2期
页 面：182-200页
核心收录：
学科分类：1002[医学-临床医学] 1001[医学-基础医学(可授医学、理学学位)] 100203[医学-老年医学] 10[医学]
基 金：supported by the National Natural Science Foundation of China(81901142) funds for key support objects of Third Military Medical University
主 题：Intermittent theta burst stimulation Alzheimer’s disease Iron-sulfur cluster assembly 1 Mitochondrial dysfunction Neurodegeneration
摘 要：Intermittent theta burst stimulation(iTBS),a time-saving and cost-effective repetitive transcranial magnetic stimulation regime,has been shown to improve cognition in patients with Alzheimer’s disease(AD).However,the specific mechanism underlying iTBS-induced cognitive enhancement remains *** studies suggested that mitochondrial functions are modulated by magnetic ***,we showed that iTBS upregulates the expression of iron-sulfur cluster assembly 1(ISCA1,an essential regulatory factor for mitochondrial respiration)in the brain of APP/PS1 *** vivo and in vitro studies revealed that iTBS modulates mitochondrial iron-sulfur cluster assembly to facilitate mitochondrial respiration and function,which is required for ***,iTBS rescues cognitive decline and attenuates AD-type pathologies in APP/PS1 *** present study uncovers a novel mechanism by which iTBS modulates mitochondrial respiration and function via ISCA1-mediated iron-sulfur cluster assembly to alleviate cognitive impairments and pathologies in *** provide the mechanistic target of iTBS that warrants its therapeutic potential for AD patients.
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