hsp90 Cochaperone FKBP51 调节 tau 结构和功能-猫眼课题宝

hsp90 Cochaperone FKBP51 调节 tau 结构和功能

批准号：

10607304

负责人：

Laura J Blair

金额：

$72.17万

依托单位：

UNIVERSITY OF SOUTH FLORIDA

依托单位国家：

美国

项目类别：

财政年份：

2011

资助国家：

美国

项目状态：

未结题

起止时间：

2011-04-01 至 2028-02-29

来源：

https://reporter.nih.gov/project-details/10607304

关键词：

Ablation Affect Affective Symptoms Aging Alleles Alzheimer&apos s Disease Alzheimer&apos s disease brain Alzheimer&apos s disease patient Attenuated Behavior assessment Behavioral Biology Brain Cognitive Cognitive deficits Data Disease Progression Electrophysiology (science)FK506 binding protein 5 Functional disorder Goals Health Immune response Impaired cognition Impairment In Vitro Individual Knockout Mice Knowledge Link MAPT gene Mediating Mental Depression Metabolism Mitochondria Modeling Molecular Molecular Chaperones Mood Disorders Mus Neurons Obesity Outcome Pathogenesis Pathologic Pathway interactions Patients Proteins Proteomics Research Respiration Risk Role Short-Term Memory Single Nucleotide Polymorphism Stress Structure Synapses Synaptic plasticity Synaptosomes Tacrolimus Binding Proteins Tauopathies Testing Toxic effect Transgenic Mice Variant Work aged excitatory neuron genetic variant hormonal signals in vivo inhibitor insight knock-down mitochondrial dysfunction mouse development mouse model neuron loss neuropathology neuropsychiatric symptom neurotoxic neurotoxicity polyglutamine resilience risk variant steroid hormone tau Proteins tau aggregation tau mutation tau-1 transcriptomics

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Project Summary/Abstract Neuropsychiatric symptoms (NPS), like depression, are common early in Alzheimer’s disease (AD) and correlate with a faster decline in patients. NPS and cognitive deficits in AD have been linked with the accumulation of tau protein. Two independent studies associated an allelic variant in the 51kDa FK506-binding protein (FKBP51) with increased risk for depression in AD. FKBP51 also regulates tau accumulation and toxicity to nerve cells. We will use transgenic mouse models to determine if either removing or inhibiting FKBP51 in mice will be protective against tau accumulation. We will also study whether mice that have this risk variant in combination with tau accumulation are more vulnerable to NPS. The critical knowledge gained through this work will add to our understanding of the role of FKBP51 in regulating tau pathogenesis especially during disease progression. This work will have a positive impact in AD research as we will further validate FKBP51 as a target and characterize the molecular landscape associated with vulnerability to NPS in tauopathies.

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