The Corces lab melds epigenomics, computational biology, large-scale screens, and single-cell technologies to study neurodegeneration. We make heavy use of primary patient tissue to form hypotheses that can be tested in cellular and organismal model systems. Our long-term research interest is to use insights from the epigenome to inform our understanding of neurological disease with the goal of identifying novel avenues for therapeutic intervention. More specifically, we are interested in how the genome and epigenome intersect and how inherited genetic variation interfaces with lived experiences and environmental factors to produce durable and functional epigenetic alterations that lead to Alzheimer’s and Parkinson’s disease.
Alzheimer’s disease (AD) and Parkinson’s disease (PD) both manifest as devastating age-related progressive neurodegeneration. This neurodegeneration and the concomitant loss of cognitive function plagues more than 44 million individuals worldwide for AD and more than 10 million individuals worldwide for PD. Our understanding of the molecular pathogenesis of these diseases remains incomplete and no therapies exist to prevent, stop, or cure the associated neurodegeneration. This marks one of the greatest unmet clinical needs of our time and a looming global public health crisis. At the most basic level, neurodegenerative diseases such as AD and PD result from the wrong genes being expressed in the wrong ways at the wrong times. Moreover, these are diseases of age with most patients manifesting symptoms after age 70. This age-associated onset of symptoms indicates that in addition to the known genetic causes of neurodegeneration, there are also epigenetic underpinnings to these diseases. This leads to the hypothesis that understanding the epigenome in AD and PD has the potential to provide key insights that inform the development of novel therapies.