Aging effects on the neural coding of proactive and reactive cognitive control: Administrative Supplement

衰老对主动和反应性认知控制神经编码的影响：行政补充

基本信息

批准号：
10715441
负责人：
TODD S BRAVER
金额：
$ 38.8万
依托单位：
WASHINGTON UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
2022
资助国家：
美国
起止时间：
2022-09-30 至 2024-08-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10715441
关键词：
Administrative Supplement Adopted Adoption Age-associated memory impairment Aging Alzheimer associated neurodegeneration Alzheimer&apos s Disease Alzheimer’s disease biomarker Amyloid Amyloid beta-Protein Anatomy Anterior Award Behavioral Biological Markers Blood Blood specimen Brain Code Cognitive aging Collaborations Color Communities Consensus Data Data Collection Development Diagnostic Dissociation Elderly Emotions Ensure Exhibits Experimental Designs Funding Future Glial Fibrillary Acidic Protein Goals Grant Human Resources Impaired cognition Impairment Intervention Laboratories Lateral Life Link Literature Mass Spectrum Analysis Methodology Methods Midbrain structure Mission Modality Nerve Degeneration Neurobiology Participant Pathologic Pathology Pattern Plasma Prefrontal Cortex Process Research Research Design Research Personnel Research Project Grants Risk Assessment Sampling Science Specificity Stimulus Subgroup Techniques Testing Thick Thinking Universities Variant Washington Well in self Work age effect age related blood-based biomarker brain behavior cingulate cortex cognitive control cognitive function cognitive neuroscience cost effective dopamine system experience falls functional magnetic resonance imaging/electroencephalography healthy aging indexing innovation magnetic resonance imaging biomarker medical schools multimodal neuroimaging multimodality neural neuroimaging marker neuromechanism novel pilot test pre-clinical preservation prospective psychologic single molecule success tau Proteins temporal measurement

项目摘要

Project Summary This proposal explores the neural and psychological mechanisms that underlie the well-established declines in cognitive control function experienced by otherwise healthy older adults. A clear consensus in the cognitive neuroscience of aging is that age-related cognitive control declines reflect neurobiological changes that occur in the functioning of the mid-brain dopamine system, interacting with targets located in the lateral prefrontal cortex (lPFC) and anterior cingulate cortex (ACC). The current proposal adopts an innovative experimental approach to this issue, by leveraging the methodology of representational similarity analysis (RSA), to examine the neural coding of cognitive control and how it changes with advancing age. Specifically, we utilize RSA to test the Dual Mechanisms of Control (DMC) theoretical framework, which postulates that older adults will exhibit clear impairments in the engagement of proactive control, but relative preservation of reactive control. The project directly tests this hypothesis, employing novel theoretically-optimized variants of the work- horse color-word Stroop paradigm, combined with RSA methods, to examine the neural mechanisms associated with proactive and reactive control, using a multi-modal neuroimaging approach involving matched fMRI and EEG studies. This multi-modal approach enables a systematic and comprehensive test of the DMC framework, to test whether proactive and reactive control have distinct temporal dynamic signatures, and involve anatomically dissociable neural mechanisms within the lPFC and ACC. We further propose to enrich our understanding of the mechanisms of age-related change in cognitive control function, by capitalizing on recent advances in the ability to assess risk of preclinical Alzheimer’s Disease (AD) and AD-related neurodegeneration through the use of blood plasma-based biomarkers. Through new collaborations with Dr. Brian Gordon, Dr. Ryan Bogdan, and Dr. Suzanne Schindler, we will utilize state-of-the-art methods, including single-molecule array (Simoa) and mass spectrometry, to comprehensively assess key blood-based biomarkers related to amyloid (APOE, beta-amyloid), tau (ptau181), and neurodegeneration (NfL, GFAP), as well as anatomical MRI biomarkers (e.g., cortical thickness). We propose an Administrative Supplement to provide additional support for us to acquire, process and rigorously analyze AD-related biomarker data. This Supplement will dramatically enhance the scope, impact, and

项目摘要该提案探讨了神经和心理机制，这些机制是公认的下降的基础其他健康的老年人经历的认知控制功能。认知明确共识衰老的神经科学是与年龄相关的认知控制下降反映了发生的神经生物学变化在中脑多巴胺系统的功能中，与位于前额叶中的靶标相互作用皮层（LPFC）和前扣带回皮层（ACC）。当前的提案采用了创新的实验通过利用代表性相似性分析（RSA）的方法来解决这个问题的方法，检查认知控制的神经编码以及它如何随着年龄的增长而变化。具体来说，我们利用 RSA测试对照双重机制（DMC）理论框架，该框架假定老年人主动控制的参与方面将存在明显的损害，但是反应性相对保留控制。该项目直接检验了这一假设，该假设采用了工作理论优化的新变体马颜色的Stroop范式与RSA方法相结合，以检查神经机制使用涉及匹配的多模式神经影像学方法，与主动和反应性控制有关 fMRI和EEG研究。这种多模式方法可以对DMC进行系统和全面的测试框架，测试主动和反应性控制是否具有不同的临时动态特征，并涉及 LPFC和ACC中的解剖学上可解散的神经机制。我们进一步提议丰富我们的通过利用最近评估临床前阿尔茨海默氏病（AD）和与广告相关的风险的能力的进步神经变性通过使用基于血浆的生物标志物。通过与博士的新合作 Brian Gordon，Ryan Bogdan博士和Suzanne Schindler博士，我们将使用最先进的方法，包括单分子阵列（SIMOA）和质谱法，以全面评估基于血液的生物标志物与淀粉样蛋白（APOE，β-淀粉样蛋白），Tau（PTAU181）和神经变性（NFL，GFAP）有关解剖学MRI生物标志物（例如皮质厚度）。我们提出了一种行政补品来提供为我们获取，处理和严格分析与广告相关的生物标志物数据的额外支持。此补充将大大提高范围，影响和