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Neurodevelopment in children from families with genetic frontotemporal dementia and Alzheimer's disease

遗传性额颞叶痴呆和阿尔茨海默病家庭儿童的神经发育

基本信息

批准号：
10632707
负责人：
SUZEE EURIE LEE
金额：
$ 3.62万
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：
2022
资助国家：
美国
起止时间：
2022-02-15 至 2027-01-31
项目状态：
未结题

来源：
https://reporter.nih.gov/project-details/10632707
关键词：
Adult Age Alzheimer&apos s Disease Amygdaloid structure Animal Model Attention Attention deficit hyperactivity disorder Behavioral Symptoms Bilateral Biological Markers Biology Brain Child Clinical Cognitive Corpus striatum structure Cross-Sectional Studies DNA Sequence Alteration Data Differential Diagnosis Disease Dominant Genes Dyslexia Family Family member Frontotemporal Dementia Functional Magnetic Resonance Imaging Genetic Human Inferior Insula of Reil Language Learning Disabilities Left Life Longevity Memory Modeling Mutation Neurobehavioral Manifestations Neurodegenerative Disorders Neurodevelopmental Disorder Pattern Performance Phase Play Primary Progressive Aphasia Resources Role Structure Symptoms Syndrome Work aged autism spectrum disorder autistic children base behavior measurement behavioral variant frontotemporal dementia disease-causing mutation early detection biomarkers executive function frontal lobe gray matter insight mutation carrier neural circuit neural network neurodevelopment neuroimaging presenilin-1 white matter young adult

项目摘要

Supplement Title: Neurodevelopment in children from families with genetic frontotemporal dementia and Alzheimer's disease Project summary/abstract: The current conceptualization of genetic frontotemporal dementia (FTD) and Alzheimer's disease (AD) is that they are neurodegenerative diseases with symptoms developing later in life. Yet, studies in animal models support the notion that autosomal dominant genes whose mutations cause these diseases play critical roles in neurodevelopment. Previous studies show that young adult presymptomatic carriers for FTD and AD mutations show detectable differences in the neural circuits that are also targeted during the symptomatic phase. It remains unknown how early these abnormalities start and the extent to which children with these mutations may show clinical overlap with neurodevelopmental disorders such as autism spectrum disorder (ASD), attention-deficit hyperactivity disorder (ADHD), and language-based learning disabilities (LBLD). Studying children with FTD and AD mutations offers a unique model to evaluate lifelong neural circuit vulnerability since each disease targets distinct neural circuits. At the UCSF Dyslexia Center, we will cross-sectionally study children from families with a known genetic mutation for FTD or AD and compare them children with ASD, ADHD, and LBLD. Aims 1 and 2 will compare children carrying a genetic mutation for FTD and children carrying a genetic mutation for AD with noncarrier family members to identify differences in brain structure and neural network connectivity. Aim 3 will explore comparisons between mutation carriers and children with ASD, ADHD, and LBLD. Upon completion, we will have identified how early disease-specific neural circuit differences arise in genetic FTD and AD. These findings will reveal important insights into the underlying biology of these diseases and when biomarker differences develop during the lifespan for genetic FTD and AD.

补充标题：遗传性额颞叶痴呆家庭儿童的神经发育