Biobehavioral basis of knee OA

膝关节骨关节炎的生物行为学基础

• 批准号: 10290392
• 负责人: Yenisel Cruz-Almeida
• 金额: $ 37.95万
• 依托单位: UNIVERSITY OF FLORIDA
• 依托单位国家: 美国
• 财政年份: 2020
• 资助国家: 美国
• 起止时间: 2020-05-15 至 2025-02-28
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/10290392
• 关键词: Absence of pain sensation; Address; Aging; Alzheimer' s Disease; Alzheimer' s disease related dementia; Area; Award; Biological Aging; Biological Markers; Brain; Brain region; Cognitive; Diagnosis; Elderly; Equilibrium; Ethnic group; Goals; Health; Human; Individual; Knee Osteoarthritis; Literature; Mediating; Methodology; Neurobiology; Nociception; Outcome; Pain; Pain intensity; Pain management; Parents; Pathway interactions; Persons; Predisposition; Process; Race; Research; Risk; Stimulus; System; Testing; biobehavior; chronic pain; cognitive function; conditioned pain modulation; conditioning; improved; multimodality; neuroimaging; pain inhibition; pain processing; pain reduction; prospective; racial and ethnic; recruit; relating to nervous system; response; spinal reflex; tool

Abstract of the proposed research that shows the relevance to AD/ADRD The susceptibility to pain depends on the balance of activity in ascending and descending pain pathways. The descending pain control system modulates pain by inhibiting or facilitating nociceptive processing. Well-established tools to study this system in humans are conditioned pain modulation (CPM) paradigms in which pain intensity ratings of test stimuli are obtained in the presence and absence of a concomitantly, remotely applied conditioning stimulus. More negative CPM responses (= reduced pain intensity ratings under concurrent stimulation) are indicative of endogenous analgesia (i.e., increased pain inhibition) and are mediated by spino-bulbo-spinal reflexes which are controlled by higher cortical brain areas. Given that the same brain regions needed for descending pain modulation are also negatively impacted in persons with Alzheimer's Disease (AD), aberrant descending pain inhibition might contribute to altered pain processing in AD. To our knowledge no studies to date have investigated descending pain inhibition in persons with AD nor its underlying mechanisms. The proposed supplement will recruit 50 older adults diagnosed with mild AD with and without pain and undergo experimental sessions of conditioned pain modulation, a cognitive function battery and multi- modal neuroimaging consistent with the methodology used in the parent R01 award and compared with individuals with knee osteoarthritis that are cognitively intact. The proposed research addresses a significant gap in the literature and would be the first to evaluate the pain-related changes in the neural substrates in older persons with and without AD in relation to pain. The identification of key top-down modulatory brain networks impacted by pain and AD will increase our understanding of neurobiological changes in pain processing that may put individuals at risk of developing AD.

拟议研究的摘要，该研究显示了与AD/ADRD的相关性 疼痛的敏感性取决于疼痛和下降疼痛的活动平衡 途径。下降的疼痛控制系统通过抑制或促进伤害性来调节疼痛 加工。在人类中研究该系统的完善工具是条件疼痛调节 （CPM）在存在下获得测试刺激的疼痛强度等级的范例，并且 缺乏伴随，远程应用的调节刺激。更多负CPM响应（= 降低并发刺激下的疼痛强度等级）表示内源性镇痛 （即增加疼痛抑制作用），并由spino-Bulbo脊柱反射介导，该反射由 较高的皮质大脑区域。鉴于下降疼痛所需的相同大脑区域 在阿尔茨海默氏病（AD）的患者中也会受到负面影响，疼痛异常 抑制作用可能导致AD中的疼痛处理改变。据我们所知，迄今尚无研究 研究了AD患者或其潜在机制的疼痛抑制作用。这 拟议的补充剂将招募50名被诊断出患有和不疼痛的轻度AD的老年人 进行条件疼痛调节，认知功能电池的实验会议和多种 模态神经影像学与父级R01奖中使用的方法一致，并与 具有认知完整的膝盖骨关节炎的人。拟议的研究解决了 文献中的显着差距，将是第一个评估神经疼痛变化的差距 与疼痛有关的老年人和没有AD的老年人的底物。钥匙自上而下的识别 受疼痛和广告影响的调节性脑网络将增加我们对神经生物学的理解 疼痛处理的变化可能会使个人有发展AD的风险。