Research Education Component

研究教育部分

基本信息

项目摘要

Mount Sinai ADRC (Sano): Research Education Component (REC) – Research Summary The Research Education Component (REC) of the Alzheimer's Research Center (ARC) will provide critically needed training for junior faculty, senior postdoctoral fellows, and clinical research track residents and fellows, to conduct research on Alzheimer's disease-related disorders (ADRD). REC will support mentored research experiences for junior investigators during two vulnerable periods of their career development, early in their careers as they approach the end of residency or fellowship training, when they are too junior to obtain career development awards, or later when they have completed a career development award (e.g. K award), have a junior faculty position, but have yet to obtain RO1 or equivalent grant funding. Through the participation of distinguished senior faculty mentors in an intellectually and technologically rich academic environment at the Icahn School of Medicine at Mount Sinai (ISMMS), REC will also provide a mechanism to support gifted and highly motivated junior investigators who are new to AD research. Complementing state-of-the-art research training with teams of multidisciplinary REC mentors, REC scholars will receive an individually tailored didactic curriculum and exposure to multiple career-building activities, including a work- in-progress seminar series, science communication course, translational neuroscience and AD seminar series, grant and publication writing workshops and course, an academic survival and leadership seminar series, optional advanced coursework in neuroscience, genetics/genomics, and quantitative analyses, and a variety of additional resources available at ISMMS. REC scholars, moreover, will take advantage of well- designed, accessible ARC cores which will assist in their training allowing timely completion of their research program milestones and assisting scholars to meet goals set in their individual development plans (IDPs). REC objectives include: (1) To support trainees to conduct research to test questions and mechanisms important to the health of ADRD patients; (2) To provide advanced training in approach and methodologies needed to conduct high quality, ethical, and multidisciplinary research on ADRD disorders; (3) To provide multidisciplinary mentorship, with at least two interdisciplinary mentors, and an individually tailored career development plan; (4) To provide multiple forums that will encourage development of trainee presentation skills. (5) To prepare and assist trainees to submit and obtain external grant funding that is appropriate for their career stage (e.g. K award for postdocs and clinical fellows, or R21/RO1 for junior faculty), to sustain long-term academic careers as independent investigators and future leaders in the basic, translational, and clinical research of ADRDs. REC leadership, mentoring teams, and of course REC scholars themselves, will work together to closely assess short-term trainee progress and outcomes, and long-term trainee career development, providing critical metrics to evaluate overall success and guide future improvement.
西奈山发展研究中心(SANO):研究教育部分(REC)--研究总结 阿尔茨海默病研究中心(ARC)的研究教育部分(REC)将提供关键的 需要对初级教员、高级博士后研究员和临床研究人员进行培训 进行阿尔茨海默病相关疾病(ADRD)的研究。REC将支持被指导 初级调查员在职业发展早期两个脆弱时期的研究经验 在他们的职业生涯中,当他们即将结束住院医生或研究员培训时,当他们太初级而不能 获得职业发展奖,或在他们完成职业发展奖(例如K ),拥有初级教师职位,但尚未获得RO1或同等的赠款资金。通过 杰出的高级教员导师参与智力和技术丰富的学术 西奈山伊坎医学院(ISMMS)的环境,REC还将提供一种机制 支持才华横溢、积极进取的初级研究人员,他们是AD研究的新手。互补 与多学科REC导师团队一起接受最先进的研究培训,REC学者将获得 个人定制的教学课程和参与多项职业发展活动,包括一部作品- 正在进行的系列研讨会、科学交流课程、翻译神经科学和AD研讨会 系列、资助和出版物写作工作坊和课程,学术生存和领导力研讨会 神经科学、遗传学/基因组学和定量分析系列选修高级课程,以及 ISMMS上提供的各种额外资源。此外,REC学者将利用好的- 设计的、可访问的ARC核心,将帮助他们进行培训,从而及时完成他们的研究 计划里程碑,并协助学者实现其个人发展计划(IDP)中设定的目标。 REC的目标包括:(1)支持受训人员进行研究,以测试问题和机制 对ADRD患者的健康非常重要;(2)提供有关方法和方法的高级培训 对ADRD障碍进行高质量、伦理和多学科研究所需的方法; (3)提供多学科指导,至少有两名跨学科导师和一名个人导师 量身定制的职业发展计划;(4)提供多个论坛,鼓励 实习生演示技巧。(5)准备和协助学员提交和获得外部赠款资金 这适合于他们的职业阶段(例如,博士后和临床研究员的K奖,或初级的R21/RO1 学院),以维持长期的学术生涯,作为独立调查人员和未来的领导者 ADRDS的基础、翻译和临床研究。REC领导力、指导团队,当然还有 REC学者本身将共同努力,密切评估受训人员的短期进展和成果, 和长期的实习生职业发展,提供关键指标来评估总体成功和指导 未来的改进。

项目成果

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NIKOLAOS K ROBAKIS其他文献

NIKOLAOS K ROBAKIS的其他文献

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{{ truncateString('NIKOLAOS K ROBAKIS', 18)}}的其他基金

Research Education Component
研究教育部分
  • 批准号:
    10614022
  • 财政年份:
    2020
  • 资助金额:
    $ 26.63万
  • 项目类别:
PS 1 activates the PI3k/Akt cell survival pathway
PS 1 激活 PI3k/Akt 细胞存活途径
  • 批准号:
    6705139
  • 财政年份:
    2004
  • 资助金额:
    $ 26.63万
  • 项目类别:
PS 1 activates the P13k/Akt cell survival pathway
PS 1 激活 P13k/Akt 细胞存活途径
  • 批准号:
    6993570
  • 财政年份:
    2004
  • 资助金额:
    $ 26.63万
  • 项目类别:
PS1 mediates the neuroprotective functions of the ephrinB/EphB system
PS1 介导 ephrinB/EphB 系统的神经保护功能
  • 批准号:
    8074904
  • 财政年份:
    2004
  • 资助金额:
    $ 26.63万
  • 项目类别:
PS1 mediates the neuroprotective functions of the ephrinB/EphB system
PS1 介导 ephrinB/EphB 系统的神经保护功能
  • 批准号:
    8271402
  • 财政年份:
    2004
  • 资助金额:
    $ 26.63万
  • 项目类别:
PS 1 activates the P13k/Akt cell survival pathway
PS 1 激活 P13k/Akt 细胞存活途径
  • 批准号:
    6836447
  • 财政年份:
    2004
  • 资助金额:
    $ 26.63万
  • 项目类别:
PS1 mediates the neuroprotective functions of the ephrinB/EphB system
PS1 介导 ephrinB/EphB 系统的神经保护功能
  • 批准号:
    8475506
  • 财政年份:
    2004
  • 资助金额:
    $ 26.63万
  • 项目类别:
PS1 mediates the neuroprotective functions of the ephrinB/EphB system
PS1 介导 ephrinB/EphB 系统的神经保护功能
  • 批准号:
    7880651
  • 财政年份:
    2004
  • 资助金额:
    $ 26.63万
  • 项目类别:
Presenilin 1 (PS1) activates the PI3k/Akt cell survival pathway
Presenilin 1 (PS1) 激活 PI3k/Akt 细胞存活途径
  • 批准号:
    7173255
  • 财政年份:
    2004
  • 资助金额:
    $ 26.63万
  • 项目类别:
VESICULAR LOCALIZATION AND FUNCTION OF PRESENILIN 1 FRAGMENT
早老素 1 片段的囊泡定位和功能
  • 批准号:
    6593367
  • 财政年份:
    2002
  • 资助金额:
    $ 26.63万
  • 项目类别:

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    2009
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Pathophysiological mechanisms of hypoperfusion in mouse models of Alzheimer?s disease and small vessel disease
阿尔茨海默病和小血管疾病小鼠模型低灌注的病理生理机制
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患有亨廷顿病的父母及其后代的社会联系和沟通:与心理和疾病进展的关联
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The Role of Menopause-Driven DNA Damage and Epigenetic Dysregulation in Alzheimer s Disease
更年期驱动的 DNA 损伤和表观遗传失调在阿尔茨海默病中的作用
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The Role of Menopause-Driven DNA Damage and Epigenetic Dysregulation in Alzheimer s Disease
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