Enhancement of neural regeneration

增强神经再生

• 批准号: 10227962
• 负责人: Christian Petersen
• 金额: $ 40.1万
• 依托单位: NORTHWESTERN UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2019
• 资助国家: 美国
• 起止时间: 2019-09-01 至 2023-07-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/10227962
• 关键词: Address; Adult; Animals; Biological; Biological Assay; Biological Models; Biology; Brain; Brain region; Bromodeoxyuridine; Cadherins; Cell Transplantation; Cells; Data; Data Set; Decapitation; Development; Disease; Engraftment; Fatty acid glycerol esters; Fluorescent in Situ Hybridization; Foundations; Genes; Genetic; Genetic Transcription; Genome; Goals; Grant; Histologic; In Situ Nick-End Labeling; Injury; Label; Lead; Location; Logic; Medical; Methods; Molecular; Molecular Target; Natural regeneration; Nerve Regeneration; Nervous System Trauma; Neurons; Organ; Organism; Pathway interactions; Phenotype; Phosphotransferases; Planarians; Platyhelminths; Process; Production; Publishing; RNA Interference; RNA interference screen; Regenerative capacity; Regulatory Pathway; Signal Transduction; Signaling Molecule; Specificity; Stains; System; TEC Protein Tyrosine Kinase; Testing; Time; Tissue Transplantation; Tissues; Transplantation; base; behavior test; cell type; experience; experimental study; gene function; information model; injury and repair; insight; mind control; neurogenesis; novel strategies; programs; receptor; regeneration model; regeneration potential; regenerative; regenerative growth; regenerative tissue; relating to nervous system; repaired; restoration; single molecule; single-cell RNA sequencing; stem cell differentiation; stem cells; targeted treatment; tissue regeneration; tissue repair; transcription factor; transcriptome

Project Summary/Abstract Organisms with regenerative abilities have been informative models for uncovering natural mechanisms by which nervous system damage activates stem or progenitor cells for injury repair. The timing, location, and extent of injuries are not predetermined, requiring the existence of mechanisms that instruct tissue restoration activities that perfectly counter the effects of damage. A key question to understand this process is how cessation of regenerative growth is accomplished. To begin to address this question, it is essential to define the transcriptional and cell signaling systems that negatively regulate adult regenerative neurogenesis. While regenerative tissues have been extensively probed for positive regulators of regeneration, much less is known about factors that act in opposition and whose inhibition could lead to enhanced neural regeneration. In the aims of this grant, this deficit is addressed by leveraging expertise in the planarian system, which uniquely allows access to the biology of complete adult brain regeneration. Uncovering the conserved and fundamental mechanisms used by organisms to limit the extent and rate of tissue regeneration and cell turnover will provide foundational insights into understanding and ultimately treating diseases characterized by an inability to undergo sufficient neural repair.

项目概要/摘要 具有再生能力的生物体已成为揭示自然机制的信息模型 神经系统损伤会激活干细胞或祖细胞进行损伤修复。时间、地点和 损伤的程度不是预先确定的，需要存在指导组织恢复的机制 完全抵消损害影响的活动。理解这个过程的一个关键问题是如何 再生生长停止。要开始解决这个问题，有必要定义 负调控成人再生神经发生的转录和细胞信号系统。尽管 再生组织已被广泛探索再生的正调节因子，但知之甚少 关于相反作用的因素以及其抑制可能导致神经再生增强的因素。在 根据这笔赠款的目标，这一赤字是通过利用涡虫系统的专业知识来解决的，该系统具有独特的 允许了解完整的成人大脑再生的生物学。揭示保守的和基本的 生物体用来限制组织再生和细胞更新的程度和速度的机制将提供 对理解和最终治疗以无法治疗为特征的疾病的基本见解 进行充分的神经修复。