Diversity Supplement-Massoudi

多样性补充-Massoudi

基本信息

批准号：
10787059
负责人：
Myriam Marianne Chaumeil
金额：
$ 10.68万
依托单位：
UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
依托单位国家：
美国
项目类别：
财政年份：
2019
资助国家：
美国
起止时间：
2019-09-18 至 2024-08-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10787059
关键词：
Acceleration Address Age Age Months Alzheimer&apos s Disease Alzheimer&apos s disease related dementia Animal Model Ascorbic Acid Association Learning Behavior Behavioral Biological Assay Biological Markers Blood Vessels CADASIL Calcium Cell Surface Receptors Cerebral small vessel disease Cerebrum Characteristics Clinical Cognitive Cognitive deficits Country Data Dedications Dementia Development Disease Disease Pathway Electrophysiology (science)Elements Ensure Etiology Evaluation Experimental Models Female Functional disorder Genes Genetic Genetic Models Goals Human Image Impaired cognition Intervention Knowledge Learning Lesion Magnetic Resonance Imaging Mediating Memory Meta-Analysis MicroRNAs Microcirculation Microvascular Dysfunction Modeling Molecular Mus Mutant Strains Mice Mutation Myography Outcome Pathogenesis Pathology Pathway interactions Phase Physiological Population Post-Transcriptional Regulation Pre-Clinical Model Preclinical Testing Prevention strategy Process Radiology Specialty Research Stroke Subgroup Syndrome Therapeutic Intervention Validation Vascular Diseases age related aged arterial tortuosity behavior test brain circulation cerebral microbleeds cerebrovascular pathology cognitive change cognitive function cohort comparative design effective intervention genetic resource genome wide association study genome-wide analysis human disease imaging modality imaging study improved innovation insight male mouse model neuropathology novel patch clamp pressure prevent prospective test receptor binding vascular cognitive impairment and dementia white matter

项目摘要

PROJECT SUMMARY Vascular cognitive impairment and dementia (VCID) is any level of cognitive alteration that is attributable to cerebrovascular pathologies. VCID is second only to Alzheimer’s disease as a cause of dementia and accounts for ~15-30% of all dementia cases. Cerebral small vessel diseases (cSVDs) are group of pathologies afflicting the microcirculation of the brain that collectively account for up to 20% of all strokes and is the most common pathology underlying VCID. The impact of cSVD and VCID is expected to increase rapidly as the population of the US and other countries ages. Importantly, the pathogeneses of cSVDs are incompletely understood which represents a major barrier in developing strategies for prevention and treatment. Research described in this proposal will develop and validate five novel mouse models of cSVD based on genes and mutations that are demonstrated to contribute to human disease. We have assembled an interdisciplinary team of experts that will integrate unique genetic resources, vascular pressure myography, patch-clamp electrophysiology, calcium imaging, specialized magnetic resonance imaging modalities and learning and memory behavior assays to develop and characterize multiple novel genetic models of cSVD using genes that contribute to disease in humans. Our long-term objective is to develop and employ genetic models that faithfully recapitulate important hallmarks of human cSVD and VCID.

项目摘要血管认知障碍和痴呆（VCID）是任何归因于认知的改变脑血管病理。 VCID仅次于阿尔茨海默氏病，是痴呆症的原因在所有痴呆症病例中约有15-30％。脑小血管疾病（CSVD）是折磨的一组病理大脑的微循环集体占所有中风的20％，是最常见的 VCID的病理学。随着人口的人口，CSVD和VCID的影响将迅速增加美国和其他国家的年龄。重要的是，CSVD的病原体尚不完全理解代表着制定预防和治疗策略的主要障碍。其中描述了提案将基于基因和突变，开发和验证五个新型CSVD小鼠模型证明有助于人类疾病。我们已经组建了一个跨学科的专家团队综合的独特遗传资源，血管压力密码，斑块钳电生理学，钙成像，专门的磁共振成像方式以及学习和记忆行为分析使用有助于疾病的基因开发和表征CSVD的多种新型遗传模型人类。我们的长期目标是开发和员工遗传模型，这些模型忠实地概括了重要的人类CSVD和VCID的标志。