Fonken Lab

The University of Texas at Austin • College of Pharmacy

How do microglia, the brains resident immune cell, shape behavior and cognition?

Microglia, were first identified in the brain by Del Rio-Hortega over 100 years ago. These cells were initially thought to have a passive role in the healthy brain and only become active during central nervous system injury. We now know that glial cells have a diverse array of functional roles in maintaining brain homeostasis and in responding to CNS pathology.

Our research focuses on understanding how endogenous (e.g. circadian rhythms and aging) and exogenous (e.g. environmental pollutants, infection, and injury) factors can lead to a primed neuroinflammatory environment resulting in cognitive and affective behavioral changes.

Our current research projects:

Over an animals’s lifespan, microglia become more reactive or “primed”, worsening outcomes when an immune challenge is encountered (e.g. infection, surgery, or injury.
In modern society, sterile conditions may actually worsen inflammation. The immune system co-evolved with microorganisms, and underexposure to these organisms can harm immune function. Controlled reintroduction of microorganisms could improve the composition of the microbiome and lessen hyperactive inflammatory responses.
The Fonken lab is investigating mechanisms by which a vaccination of the soil bacterium, Mycobacterium vaccae, prevents exacerbated neuroinflammatory and behavioral deficits in aging.
This work is supported by NIH R01 AG062716
The circadian clock is a critical regulator of biological processes, generating cycles of hormone release, sleep-wake behaviors, and timing of cell division and repair. Microglia also express circadian timekeeping mechanisms, leading to daily cycles of high and low immune reactivity. With aging and Alzheimer’s Disease (AD), these rhythms dampen, possibility contributing to heightened neuroinflammation and pathology.
The Fonken lab is investigating how circadian rhythms in immune cell trafficking may become disrupted with age and AD-like pathology.
This work is supported by start NIH R01 AG078758

Want to delve deeper?

Here are a few publications that give a good overview of our research:

Fonken et al., 2018. Mycobacterium vaccae immunization protects aged rats from surgery-elicited neuroinflammation and cognitive dysfunction. (Link)

Fonken et al., 2016. The alarmin HMGB1 mediates age-induced neuroinflammatory priming. (Link)

Fonken et al., 2015. Microglia inflammatory responses are controlled by an intrinsic circadian clock. (Link)

Fonken et al., 2011. Air pollution impairs cognition, provokes depressive-like behaviors, and alters hippocampal cytokine expression and morphology. (Link)

Fonken et al., 2010. Light at night increases body mass by shifting the time of food intake. (Link)

all publications @ pubmed