Our Trainees

Kelsey Campbell in front of her computer in the lab.

Spotlight: Kelsey Campbell

My name is Kelsey Campbell, I’m a second-year graduate student in the department of neuroscience, and I’m working in Dr. Daniel Lee’s lab studying the effects of impacted nutrient signaling in Alzheimer’s disease (AD). I grew up in south-eastern Kentucky, and there I witnessed how a dementia diagnosis was capable of altering the dynamics of my family. ... This increase in AD prevalence as lifespans increase highlights how crucial the need for research and developments in AD are. My research aims to understand how nutrient signaling effects accumulation and clearance of neurodegenerative pathology in AD, and if autophagic or lysosomal pathways can be exploited to reduce AD pathology.

Jessica Gebhart

Spotlight: Jessica Gebhardt

My name is Jessica Gebhardt, and I am a graduate student in Dr. Josh Morganti’s Lab studying the effects of dysregulated neuroinflammation following traumatic brain injury (TBI). TBI has personally impacted me and my family, and as a result I have been interested in furthering my understanding of the mechanisms underlying the injury for many years. This led me to pursue a career as a scientist focused on studying TBI. Currently, there are no cures for TBI, and treatment is limited to managing symptoms. My research seeks to target the underlying causes of prolonged symptoms after injury which will hopefully aid in the collaborative scientific endeavor to create a cure for traumatic brain injury.

Nick Devanney working in the lab

Spotlight: Nick Devanney

Nick’s project in the Johnson lab seeks to marry two facets of APOE’s risk through the concept of ‘immunometabolism’. Immunometabolism is the principle that immune cells such as microglia critically rely on metabolic pathways to perform their immune functions. Pro-inflammatory phenotypes are supported by an increased rate of the glycolysis pathway, whereas anti-inflammatory phenotypes require enhanced mitochondrial respiration. Microglia with defective mitochondria fail to engage an anti-inflammatory response.