Lifespan extension, Somatotropic signaling and Tauopathy

点击翻译按钮获取中文摘要

Tauopathies are a class of neurodegenerative diseases characterized by accumulation of abnormal and hyperphosphorylated tau protein in the brain including Alzheimer's disease (AD), Parkinson's disease (PD), Frontotemporal dementia (FTD), and Motor Neuron Disease (MND). Tauopathies occur primarily in elderly population and incidence rises with increasing age. Unfortunately, the mechanisms for the age-dependent onset of tauopathies are unknown and there are no effective therapeutic strategy. Aging is the biggest risk factor for tauopathies related disorders, suggesting that molecular alterations contributing to the aging process may represent common mechanisms for tau pathology. Employing the pathways that could slow or delay the aging process may offer novel targets for new therapeutic strategies. Murine mutant mice with slow rates of aging and murine tauopathy models with varying phenotypic effects provide the opportunity to develop novel genetic models that will allow studying the interaction of aging and tauopathy. Our proposal is to elucidate the role of the somatotropic axis in the age-dependent susceptibility to tauopathies. Our study will generate new models to study the interaction of aging with neurodegenerative diseases in the context of mutations that slow the aging process.