Our laboratory is focused on identifying common pathological mechanisms across a spectrum of disorders. In particular, the overall goal of the laboratory is to provide new insight into pathogenic mechanisms of Alzheimer's disease (AD) and related disorders and elucidate novel therapeutic strategies to treat them. To achieve these goals, the lab uses cell and animal models, as well as human biofluids and postmortem tissue samples.
Main focus areas
• Evaluating mechanisms of neurodegeneration in tauopathy. Accumulation of the tau protein is a major pathological hallmark of AD and other neurodegenerative diseases classified as tauopathies, but the mechanisms of tau aggregation and resultant toxicity remain unclear. To investigate pathogenic mechanisms common across tauopathies, our lab develops and applies new mouse models of familial and sporadic disease, followed by validation of novel discoveries in human cell models and tissue samples.
• Investigating white matter abnormalities in neurodegeneration. Defects in myelination are a common pathological feature of AD and related disorders, but the involvement of myelin-producing cells in the brain (oligodendrocytes) and their precursors in disease pathogenesis remains relatively unexplored. Our lab aims to provide new insight into the role of oligodendrocyte lineage cells in neurodegeneration.
• Defining the role of noncanonical translation in aging and the pathogenesis of AD and related disorders. The human genome consists of both coding and non-coding regions, that are distinguished by the ability to generate or code for proteins. However, while recent work has uncovered evidence that new proteins can be produced from regions of the genome previously thought to be non-coding, the ability to detect these new proteins is currently limited. Our lab is working on the generation of new datasets and research tools to improve detection of proteins derived from non-coding portions of the genome, and test their potential involvement in modulating susceptibility to aging-related conditions, such as AD.
