Rebekah Evans, PhD

Investigator:

Rebekah Evans, PhD

Name of Institution:

Georgetown University, Washington DC

Project Title:

Defining circuit alterations that influence dopaminergic neuron vulnerability in early Parkinson’s disease


Investigator Bio:

Rebekah Evans is an assistant professor at Georgetown University. She completed her PhD in neuroscience at George Mason University in Virginia with Dr. Kim Blackwell and her post-doctoral work in the National Institute of Neurological Disorders and Stroke at NIH with Dr. Zayd Khaliq. In her current research, she uses electrophysiology and two-photon imaging to understand how the structures that degenerate in Parkinson’s disease (PD) are interconnected.

Objective:

To determine how circuit alterations can increase or decrease the vulnerability of dopaminergic neurons.

Background:

PD progresses through the brain from region to region. The mechanisms of this progression are an area of active research, but how PD ultimately reaches the dopaminergic neurons remains unknown. The pedunculopontine nucleus (PPN) degenerates in PD and contains neurons which connect directly to the dopaminergic neurons. Lesions of certain subsets of PPN neurons can cause dopaminergic degeneration and can recapitulate symptoms of early PD. However, the key unanswered questions is: How does neurodegeneration in the PPN increase dopaminergic neuron vulnerability?

Methods/Design:

We will selectively lesion the cholinergic neurons of the PPN and measure cellular and circuit-level changes that occur in dopaminergic neurons. Specifically, we will use electrophysiology, two-photon imaging, and optogenetics to analyze characteristics that may influence their vulnerability to neurodegeneration such as alterations in calcium influx and excitatory input.

Relevance to Diagnosis/Treatment of Parkinson’s disease:

Understanding how early degeneration of non-dopaminergic brain structures can alter the vulnerability of dopaminergic neurons is a first step toward developing circuit-based therapies to slow the progression of PD through the brain.