Enhancing gamma band response to improve working memory in individuals with mild cognitive impairment

增强伽马带反应以改善轻度认知障碍患者的工作记忆

基本信息

批准号：
10370329
负责人：
Fiza Singh
金额：
$ 67.31万
依托单位：
UNIVERSITY OF CALIFORNIA, SAN DIEGO
依托单位国家：
美国
项目类别：
财政年份：
2020
资助国家：
美国
起止时间：
2020-04-01 至 2025-03-31
项目状态：
未结题

来源：
https://reporter.nih.gov/project-details/10370329
关键词：
Accounting Activities of Daily Living Adult Affect Alzheimer&apos s Disease Alzheimer&apos s disease model Alzheimer&apos s disease patient American Amyloid beta-42 Amyloid beta-Protein Amyloid beta-Protein Precursor Animal Model Animals Anxiety Area Attention Attention deficit hyperactivity disorder Back Base of the Brain Binding Biological Markers Brain Brain region Butyric Acids Centers for Disease Control and Prevention (U.S.)Characteristics Child Clinical Cognition Cognition Disorders Cognitive deficits Computers Dementia Disease Disease Progression Dose Down Syndrome Early identification Effect Modifiers (Epidemiology)Elderly Electroencephalography Eye Frequencies Genetic Genetic Risk Histopathology Impaired cognition Impairment Individual Interneurons Intervention Mediating Mediator of activation protein Memory Memory impairment Mental Depression Metaphor Neocortex Neurobiology Neurodegenerative Disorders Neurons Neuropsychological Tests Participant Patients Phase Photic Stimulation Placebos Play Population Prediction of Response to Therapy Prefrontal Cortex Public Health Randomized Reading Reporting Research Research Personnel Risk Risk Factors Role Senile Plaques Short-Term Memory Synaptic plasticity Techniques Testing Training Programs Visual amnestic mild cognitive impairment apolipoprotein E-4 base cognitive load cognitive reserve cost economic impact efficacy testing frontal lobe functional disability high risk hippocampal pyramidal neuron improved indexing mild cognitive impairment multisensory neural circuit neural network neurofeedback neuromechanism neuron loss neuroregulation novel post intervention prevent primary outcome recruit relating to nervous system response risk variant secondary outcome tau Proteins tau-1 therapy development treatment response

项目摘要

Abstract Alzheimer’s disease (AD) is the clinical manifestation of a neurodegenerative disorder characterized by pervasive and progressive cognitive decline with impairment in activities of daily living. According to the Centers for Disease Control the number of Americans with Alzheimer’s disease or dementia will grow to 13.9 million (2018 report) by 2060, making it an urgent public concern. Research in the last decade has focused on early identification of the disease and revealed a prodromal phase prior to the onset of functional impairments, known as mild cognitive impairment (MCI). Despite early identification, there are few treatment options to slow down progression from MCI to AD. Recent studies suggest that cognitive deficits may arise from abnormal synchronization of distributed neural networks. Synchronization or synchronous firing of neurons, binds cortical areas into functional networks in a task and state-dependent manner. Specifically, neural synchrony in the gamma band (30-45Hz) plays a central role in top-down attention, multisensory processing, perceptual binding and working memory (WM) in healthy individuals. Gamma band responses (GBR) are impaired in individuals with AD spectrum disorders, and animal studies in AD models targeting GBR have shown positive effects on cognition. Thus, developing similar treatments targeting GBR are expected to improve cognition in individuals with MCI. Our group has administered EEG-neurofeedback (EEG-NFB) targeting GBR in SCZ patients, with promising early results (research strategy). NFB is a low-cost, safe, easily administered closed-loop neuromodulation technique where subjects are shown their brain activity as a visual metaphor and asked to modulate it in a given direction. EEG- NFB has been employed in multiple disorders ranging from ADHD, depression, to anxiety and in multiple populations including children and older adults. Based on these encouraging results, we are proposing a study to 1) test the efficacy of EEG-NFB targeting GBR in individuals with amnestic MCI compared to a sham/placebo, 2) explore the mechanism underlying change in cognition and 3) explore pre-treatment characteristics that predict treatment response.

抽象的阿尔茨海默氏病（AD）是神经退行性疾病的临床表现，其特征是日常生活活动的普遍性和进步的认知能力下降。根据疾病控制中心患阿尔茨海默氏病或痴呆症的美国人数量将增长到13.9 到2060年，百万（2018年报告），使其成为紧迫的公众关注。过去十年的研究重点是早期鉴定该疾病，并在功能障碍发作之前揭示了前途阶段称为轻度认知障碍（MCI）。尽管早期识别，但很少有速度的治疗选择从MCI到AD的下降。最近的研究表明，认知定义可能来自异常分布式神经网络的同步。神经元的同步或同步触发，将皮质区域结合到任务中的功能网络和国家依赖的方式。具体而言，伽马频段（30-45Hz）中的神经同步起着核心作用在自上而下的注意力，多感官处理，感知结合和工作记忆（WM）中个人。 AD频谱障碍的个体和动物的个体中伽马频带反应（GBR）受损靶向GBR的AD模型的研究对认知显示了积极影响。那，发展相似靶向GBR的治疗方法有望改善MCI患者的认知。我们的小组有靶向SCZ患者GBR的EEG-否反馈（EEG-NFB），有望尽早结果（研究策略）。 NFB是一种低成本，安全，易于施用的闭环神经调节技术，其中将受试者显示为视觉隐喻，并被要求朝给定的方向调节。脑电 NFB已被雇用多种疾病，从多动症，抑郁，动画和多种疾病不等包括儿童和老年人在内的人群。基于这些令人鼓舞的结果，我们提出了一项研究至1）测试与A的EEG-NFB靶向GBR的EEG-NFB与A相比假/安慰剂，2）探索认知变化的机制和3）探索预处理预测治疗反应的特征。