Our Mission

Our ultimate mission is to make discoveries that will lead to improved therapies for blinding diseases and other neurological disorders. To get there, we will use interdisciplinary approaches to rigorously study the molecular basis of disease. We assert that to understand disease it must be studied at the cellular level. Neurons in the brain are remarkably diverse and comprise cell types that each have distinct molecular, physiological, and morphological characteristics. We are currently studying the interaction between cell type and disease pathology in multiple degenerative models.

Our Research

Retina Research

Retina, an approachable part of the brain

The retina has been used since the time of Ramón y Cajal to study basic principles of neurobiology. It is more experimentally tractable than the rest of the brain and there is an abundance of molecular and genetic tools to target specific neuronal populations. We have been using single-cell RNA-sequencing (scRNA-seq) to develop a comprehensive cellular atlas of all mouse retinal cell types, demonstrating that the retina is similarly complex to the rest of the brain (~130 cell types). Utilizing this "fully resolved" tissue, we are now positioned to ask how cell types differentiate during development and how they are affected by disease.

Selective Vulnerability

Selective vulnerability in neurodegeneration

A common phenomenon in neurodegenerative disorders is that certain cell types are more affected than others, even when perturbation is shared. We are using single-cell genomics to dissect what happens in different neuronal populations during neurodegeneration. By determining gene expression patterns correlating with resilience and susceptibility, we seek to identify targets for therapeutic intervention. We are currently focused on studying the selective vulnerability of retinal ganglion cells in optic neuropathies like glaucoma.

Neuroprotection Research

Neuroprotection and axon regeneration

Neurons in the central nervous system have limited potential to recover from damage to their axons. If not repaired, axonal injury can lead to cellular degeneration and functional loss. Thus, identifying ways to protect neurons and stimulate axon regeneration could hold tremendous clinical value. However, current neuroprotective and regenerative treatments fall woefully short of recovery, often only promoting survival and regeneration of a small set of neurons. Why do some neurons respond while others continue to degenerate? We are studying the cell-type specific effects of treatments to determine what differentiates the responders from the non-responders. Our goal is to design treatments that work more effectively across neuronal populations and promote functional recovery.