The contribution of premotor cortex to recovery after stroke.
前运动皮层对中风后恢复的贡献。
基本信息
- 批准号:10720483
- 负责人:
- 金额:$ 44.92万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2023
- 资助国家:美国
- 起止时间:2023-08-21 至 2027-05-31
- 项目状态:未结题
- 来源:
- 关键词:AffectAgonistAmericanAnatomyAnimal ModelAnimalsAreaBasic ScienceBehavioralBilateralBrainBrain InjuriesBrain regionChronicClinicalContinuous InfusionCoupledDistantGABA-A ReceptorGoalsHealthImplantIndividualInjuryInterventionLeftLesionLocationLong-Term CareMeasurementMeasuresMediatingMicroelectrodesModelingMotorMotor ActivityMotor CortexMovementMuscimolNeuronal PlasticityNeuronsOutcomePerformancePersonsPhysiologicalPlayPopulationProcessPublic HealthQuality of lifeRattusRecoveryRecovery of FunctionRehabilitation therapyResearchRoleScienceShapesSpeedSpinal CordStrokeStructureTimeTracerTrainingTranslatingUnited Statesbehavioral outcomecritical perioddisabilityexperiencefunctional disabilityhemiparesisimprovedin vivoinjury recoveryinnovationischemic injurymedical complicationmotor controlmotor disordermotor function recoverymotor impairmentmotor recoverymotor rehabilitationmuscle strengthneuralneural tractneurite growthnovelnovel therapeuticspost strokepre-clinicalresearch studyresponseskillssomatosensory
项目摘要
Project Summary/Abstract
The goal of this project is to determine how ipsilesional premotor cortex facilitates recovery of motor function
after ischemic injury in primary motor cortex. When an individual suffers damage to primary motor cortex, they
often experience permanent reductions in motor function, including decreased motor coordination, muscle
strength, movement speed and movement accuracy. While some spontaneous recovery can occur during the
ensuing weeks to months, functional impairments often persist, leading to a reduction in quality of life and an
increase in prolonged medical complications and expenses. Over the past two decades, basic research studies
in pre-clinical animal models of brain injury, as well as clinical populations, have suggested that the brain can
undergo structural and functional reorganization within and between spared regions. This neuroplasticity is
thought to underpin functional recovery, however its manifestation as increases in task-related motor function
has yet to be established. We have proposed that when primary motor cortex is damaged through ischemic
injury, spared sensorimotor areas can take over some volitional control of motor function, and that the ipsilesional
premotor cortex plays the biggest role in this control. In this project, we will investigate the timing and contribution
of premotor cortex on both spontaneous motor recovery and recovery facilitated by rehabilitative intervention in
a rat model of ischemic injury. First, we will establish the time period when premotor cortex contributions are
necessary for spontaneous recovery to occur by temporarily inactivating premotor cortex after the ischemic injury
(Aim 1). We will then determine if the task-related activity within premotor cortex is altered following the injury,
whether these alterations impact the population level encoding of these tasks, the role rehabilitation has in
shaping any novel task related activity and, if PM is inactivated, if task-related motor encoding occurs in other
cortical areas (Aim 2). Finally, we will establish the relationship between the timing of premotor cortex
reorganization and the strength of functional connectivity between spared areas using a stimulation-evoked
cortical connectivity measurement and then determine if this physiological marker matches the novel anatomical
sprouting from premotor cortex that occurs after an ischemic injury (Aim 3). This project is innovative as it uses
a within-animal model to assess 1) how different cortical areas reorganize to restore motor function and 2) the
impact of rehabilitation therapy on this reorganization. This project has a significant potential health impact, as
the elucidation of location, timing and mechanisms related to functional behavioral recovery, especially when
coupled to rehabilitative therapy, will create a complete picture of the neural substrates of recovery. This
information is critical to maximize existing therapies and give rise to novel applications for the treatment of brain
injuries.
项目概要/摘要
该项目的目标是确定同病前运动皮层如何促进运动功能的恢复
初级运动皮层缺血性损伤后。当一个人的初级运动皮层受到损害时,他们
经常会出现运动功能永久性下降,包括运动协调性下降、肌肉
力量、动作速度和动作精度。虽然在此期间可能会发生一些自发恢复
在接下来的几周到几个月内,功能障碍往往持续存在,导致生活质量下降和
长期医疗并发症和费用增加。近二十年来,基础研究
在脑损伤的临床前动物模型以及临床人群中,表明大脑可以
在受灾地区内部和之间进行结构和功能重组。这种神经可塑性是
被认为支持功能恢复,但其表现为任务相关运动功能的增加
尚未确定。我们提出,当初级运动皮层因缺血而受损时
受伤后,幸存的感觉运动区域可以接管一些运动功能的意志控制,并且同损伤的感觉运动区域可以接管运动功能的一些意志控制。
前运动皮层在这种控制中发挥着最大的作用。在这个项目中,我们将调查时间安排和贡献
运动前皮层对自发运动恢复和康复干预促进的恢复的影响
大鼠缺血性损伤模型。首先,我们将确定前运动皮层贡献的时间段
缺血性损伤后,通过暂时失活前运动皮层来实现自发恢复所必需的
(目标 1)。然后我们将确定前运动皮层内与任务相关的活动在受伤后是否发生改变,
这些改变是否会影响这些任务的人口水平编码,康复在其中的作用
塑造任何新的任务相关活动,如果 PM 失活,如果任务相关的运动编码发生在其他
皮质区域(目标 2)。最后,我们将建立前运动皮层时序之间的关系
使用刺激诱发的重组和备用区域之间的功能连接强度
皮质连接测量,然后确定该生理标记是否与新的解剖结构相匹配
从缺血性损伤后发生的运动前皮层发芽(目标 3)。该项目具有创新性,因为它使用了
动物内模型用于评估 1) 不同的皮质区域如何重组以恢复运动功能以及 2)
康复治疗对这种重组的影响。该项目具有重大的潜在健康影响,因为
阐明与功能性行为恢复相关的位置、时间和机制,特别是当
与康复治疗相结合,将创建康复神经基础的完整图景。这
信息对于最大化现有疗法并产生脑部治疗的新应用至关重要
受伤。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
数据更新时间:{{ journalArticles.updateTime }}
{{
item.title }}
{{ item.translation_title }}
- DOI:
{{ item.doi }} - 发表时间:
{{ item.publish_year }} - 期刊:
- 影响因子:{{ item.factor }}
- 作者:
{{ item.authors }} - 通讯作者:
{{ item.author }}
数据更新时间:{{ journalArticles.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ monograph.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ sciAawards.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ conferencePapers.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ patent.updateTime }}
DAVID GUGGENMOS其他文献
DAVID GUGGENMOS的其他文献
{{
item.title }}
{{ item.translation_title }}
- DOI:
{{ item.doi }} - 发表时间:
{{ item.publish_year }} - 期刊:
- 影响因子:{{ item.factor }}
- 作者:
{{ item.authors }} - 通讯作者:
{{ item.author }}
{{ truncateString('DAVID GUGGENMOS', 18)}}的其他基金
Shaping Motor Recovery After Stroke Using Activity-Dependent Stimulation
使用活动依赖性刺激塑造中风后运动恢复
- 批准号:
9789677 - 财政年份:2018
- 资助金额:
$ 44.92万 - 项目类别:
Shaping Motor Recovery After Stroke Using Activity-Dependent Stimulation
使用活动依赖性刺激塑造中风后运动恢复
- 批准号:
9676722 - 财政年份:2018
- 资助金额:
$ 44.92万 - 项目类别:
相似国自然基金
Agonist-GPR119-Gs复合物的结构生物学研究
- 批准号:32000851
- 批准年份:2020
- 资助金额:24.0 万元
- 项目类别:青年科学基金项目
相似海外基金
S1PR1 agonistによる脳血液関門制御を介した脳梗塞の新規治療法開発
S1PR1激动剂调节血脑屏障治疗脑梗塞新方法的开发
- 批准号:
24K12256 - 财政年份:2024
- 资助金额:
$ 44.92万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
AHR agonistによるSLE皮疹の新たな治療薬の開発
使用 AHR 激动剂开发治疗 SLE 皮疹的新疗法
- 批准号:
24K19176 - 财政年份:2024
- 资助金额:
$ 44.92万 - 项目类别:
Grant-in-Aid for Early-Career Scientists
Evaluation of a specific LXR/PPAR agonist for treatment of Alzheimer's disease
特定 LXR/PPAR 激动剂治疗阿尔茨海默病的评估
- 批准号:
10578068 - 财政年份:2023
- 资助金额:
$ 44.92万 - 项目类别:
AUGMENTING THE QUALITY AND DURATION OF THE IMMUNE RESPONSE WITH A NOVEL TLR2 AGONIST-ALUMINUM COMBINATION ADJUVANT
使用新型 TLR2 激动剂-铝组合佐剂增强免疫反应的质量和持续时间
- 批准号:
10933287 - 财政年份:2023
- 资助金额:
$ 44.92万 - 项目类别:
Targeting breast cancer microenvironment with small molecule agonist of relaxin receptor
用松弛素受体小分子激动剂靶向乳腺癌微环境
- 批准号:
10650593 - 财政年份:2023
- 资助金额:
$ 44.92万 - 项目类别:
AMPKa agonist in attenuating CPT1A inhibition and alcoholic chronic pancreatitis
AMPKa 激动剂减轻 CPT1A 抑制和酒精性慢性胰腺炎
- 批准号:
10649275 - 财政年份:2023
- 资助金额:
$ 44.92万 - 项目类别:
Investigating mechanisms underpinning outcomes in people on opioid agonist treatment for OUD: Disentangling sleep and circadian rhythm influences on craving and emotion regulation
研究阿片类激动剂治疗 OUD 患者结果的机制:解开睡眠和昼夜节律对渴望和情绪调节的影响
- 批准号:
10784209 - 财政年份:2023
- 资助金额:
$ 44.92万 - 项目类别:
A randomized double-blind placebo controlled Phase 1 SAD study in male and female healthy volunteers to assess safety, pharmacokinetics, and transient biomarker changes by the ABCA1 agonist CS6253
在男性和女性健康志愿者中进行的一项随机双盲安慰剂对照 1 期 SAD 研究,旨在评估 ABCA1 激动剂 CS6253 的安全性、药代动力学和短暂生物标志物变化
- 批准号:
10734158 - 财政年份:2023
- 资助金额:
$ 44.92万 - 项目类别:
A novel nanobody-based agonist-redirected checkpoint (ARC) molecule, aPD1-Fc-OX40L, for cancer immunotherapy
一种基于纳米抗体的新型激动剂重定向检查点 (ARC) 分子 aPD1-Fc-OX40L,用于癌症免疫治疗
- 批准号:
10580259 - 财政年份:2023
- 资助金额:
$ 44.92万 - 项目类别:
Fentanyl Addiction: Individual Differences, Neural Circuitry, and Treatment with a GLP-1 Receptor Agonist
芬太尼成瘾:个体差异、神经回路和 GLP-1 受体激动剂治疗
- 批准号:
10534864 - 财政年份:2023
- 资助金额:
$ 44.92万 - 项目类别:














{{item.name}}会员




