通过 AKAP 锚定的钙调神经磷酸酶进行淀粉样蛋白突触后信号传导-猫眼课题宝

通过 AKAP 锚定的钙调神经磷酸酶进行淀粉样蛋白突触后信号传导

批准号：

9180008

负责人：

MARK L DELL'ACQUA

金额：

$23.33万

依托单位：

UNIVERSITY OF COLORADO DENVER

依托单位国家：

美国

项目类别：

财政年份：

2016

资助国家：

美国

项目状态：

已结题

起止时间：

2016-07-01 至 2018-06-30

来源：

https://reporter.nih.gov/project-details/9180008

关键词：

A kinase anchoring protein Adult Age Aging Alzheimer&apos s Disease Amyloid Amyloid beta-Protein Amyloid beta-Protein Precursor Brain Calcineurin Calcineurin inhibitor Calmodulin Cell Nucleus Chromosomes, Human, Pair 21 Chronic Conflict (Psychology)Cyclic AMP Cyclic AMP-Dependent Protein Kinases Data Dementia Dendritic Spines Development Diagnostic Docking Down Syndrome Drug Targeting Equilibrium Excision Excitatory Synapse Functional disorder Future Gene Expression General Population Genes Genetic Transcription Genetically Engineered Mouse Glutamate Receptor Hippocampus (Brain)Human Human Chromosomes Impaired cognition Individual Inherited Intellectual functioning disability Knock-in Mouse Laboratories Learning Light Link Long-Term Depression Long-Term Potentiation Mediating Memory Memory impairment Molecular Mus N-Methylaspartate Nerve Degeneration Neuronal Dysfunction Neuronal Plasticity Neurons Nuclear Translocation PPP3CA gene Pathology Pathway interactions Phenotype Phosphorylation Phosphotransferases Presenile Alzheimer Dementia Protein Dephosphorylation Protein Fragment Proteins Publishing Receptor Activation Regulation Reporting Research Rodent Rodent Model Role Scaffolding Protein Signal Pathway Signal Transduction Synapses Synaptic plasticity T cell regulation Testing Vertebral column abstracting calcineurin phosphatase cognitive function early onset innovation interest mouse model new therapeutic target novel novel diagnostics nuclear factors of activated T-cells overexpression postsynaptic prevent receptor response synaptic depression synaptic function targeted treatment tau Proteins transcription factor voltage

项目摘要

项目成果

MARK L DELL'ACQUA的其他基金

相似基金

相关文献

中文摘要

翻译

点击翻译按钮获取中文摘要

英文摘要

Project Summary Abstract Amyloid Beta Postsynaptic Signaling through AKAP-anchored Calcineurin A overproduction from APP is believed to contribute to impaired synaptic plasticity and decreased cognitive function in Alzheimer’s disease (AD). Individuals with Down syndrome (DS; trisomy 21) have an extra copy of APP that predisposes them to early-onset AD. Thus, elucidating how A inhibits plasticity is important for understanding cognitive impairments associated with the development of dementia in AD and DS and could identify novel drug targets, diagnostics, and therapies. Rodent model studies indicate that calcineurin (CaN) phosphatase signaling could contribute to altered LTP/LTD synaptic plasticity, dendritic spine loss, and learning and memory impairments in AD. A-induced spine loss may be further linked to altered gene expression through CaN activation of the transcription factor NFAT. Here we propose to test the novel hypotheses that AKAP79/150-CaN anchoring is required for A activation of CaN signaling that regulates the balance between LTP/LTD signaling and NFAT transcription associated with dendritic spine/synapse loss.

期刊论文(0)

专著(0)

科研奖励(0)

会议论文