Grant: Travel Awards - Institute Community Support

Tauopathies are a diverse group of age-related dementia characterized by filamentous tau lesions in brain. Alzheimer's disease and Pick's disease are examples of tauopathies that have presented a tremendous challenge to health care systems worldwide. Genetically, tauopathies often do not run in families and are therefore described as 'sporadic', which is typically encountered in late adulthood. Although chronological age has been reported to be the greatest risk factor of sporadic tauopathies, very little is known about how aging gives rise to the pathology at a molecular level. The overarching goal of my research is to visualize the initial aging-related molecular events that result in sporadic tauopathies, in models that can mimic the physiology of normally aged human central nervous system. To achieve this, we can take advantage of the mutation of Hutchinson Gilford progeria syndrome (mutant protein termed 'progerin'), a lethal condition associated with accelerated aging. By artificially introducing the progeric mutations into cell models of tauopathies, we can construct a molecular environment that, to a large extent, mimics natural aging. Then by assessing initial aging-induced pathology, we may tease apart the complexity in its sporadic nature of tauopathies, which may provide insights into the development of new disease models and early disease intervention.