Research Interests

  • Cerebral ischemia and traumatic brain injury
  • Neuroinflammation and neurodegeneration
  • Sex and gender differences in response to brain damage
  • Brain-liver axis ~ Brain-gut-microbiome axis ~ Brain-periphery axis
  • Glia activation
  • Neuroprotection and Neurorestoration
  • Neurodegenerative process

Research Methods

  • Animal models of brain injury
  • In vivo imaging
  • Immunohistochemistry and microscopy analysis
  • Protein analysis
  • DNA and RNA purification
  • Sequencing and bioinformatic analysis
  • Behavior analysis

Publications on these Topics:

Stroke/brain Ischemia

Traumatic brain injury

Current Projects

The Villapol Laboratory is interested in developing novel therapies for patients suffering from brain injury while performing exploratory research in the avenue of brain trauma and stroke. The central areas of investigation include the following topics:

Nano-Neurothecnology AND Brain injury. First Biological responders

Unconventionally acquired brain injury (UBI) from focused ultrasound (FUS) and electromagnetic (EM) sources have become an emerging threat to service members and diplomats. As a result, it has become critical to understand the immediate physiological responses to UBI so that real-time monitoring and intervention systems can be developed to detect and treat these injuries promptly. Because the pathophysiology of UBI is poorly understood, to identify biomarkers that rapidly indicate UBI, we must perform high-speed, high-resolution measurements of a large variety of biomarkers over multiple modalities.

Our goal is to identify critical biochemical and biophysical markers that respond within seconds to UBI from militarily relevant energy sources and determine if the identified first biological responders depend on the energy source.

The Role of Peripheral Inflammation on Brain Damage

Traumatic Brain Injury (TBI) and cerebral ischemia trigger a loss of brain tissue and, subsequently, a strong inflammatory response in the brain. In addition, brain damage can alter the function of peripheral regions and other organs, eliciting systemic responses, and global consequences. A focal injury to the brain elicits a rapid hepatic response; the production of chemokines by the liver acts as an amplifier of the focal injury response providing a route of CNS-liver communication. However, little is currently known regarding the inflammatory mediators and acute-phase proteins involved in the peripheral regions after brain injury, such as the liver. Furthermore, the extent of damage TBI inflicts on the peripheral organs remains largely unexplored.

Can a concussion change your gut microbiota?

Athletes who participate in contact sports are at risk of suffering from concussions, which can result in chronic headaches, nausea, anxiety and depression. Head injury also induces intestinal changes, including to microbes found in the gut; and the brain, in turn, can react to signals from the intestinal microbiome. This interaction is called the “brain-gut” axis. The results from this study will help us to identify temporal sequelae and biomarkers of head injury and will lead us to new treatments to prevent the consequences of concussions.

Biomimetic Nanoparticles as a Theranostic Tool for Traumatic Brain Injury

Nanoparticles (NPs) have been used in multiple diseases as drug delivery tools with remarkable success due to their rapid diffusion and specificity in the target organ. We fabricated leukocyte-based biomimetic NPs as a theranostic tool to directly access inflamed regions in a TBI mouse model.

The Role of Microbiome in the Neuropathology of Traumatic Brain Injury and Stroke

Gut microbiota are an essential neuromodulator of gut-brain axis signaling and can impact brain inflammation and outcome after ischemic injury. Several studies have shown that microbiota composition, diversity, and richness can influence anxiety and depressive behaviors. The Villapol Lab has recently been focused on how TBI affects the function of peripheral systems and is studying how the brain injury alters the microbiome and the resultant impact on TBI-induced affective disorders.

Precision-based microbiota therapy for Alzheimer’s disease.

This study aims to investigate the mechanistic linkage between gut microbiota and Alzheimer’s disease (AD) progression following brain trauma and to explore potential interventions strategies, based on four key ideas: 1) brain damage aggravates the pathology of dementia and AD, 2) the cascade triggered after brain injury causes intestinal damage, inflammation and changes in the microbiota, 3) microbiome dysbiosis produces an increase in toxic gut metabolites that aggravate AD pathology, 4) by correcting and restoring the gut microbiota, we are modulating one of the main regulatory pathways of the immune response, and therefore, we are peripherally protecting the brain from consequent neurodegenerative processes.

Epigenomic memory of estrogen in Alzheimer’s disease.

Women’s pregnancy and reproductive history affect their susceptibility to Alzheimer’s disease (AD). The number of pregnancies or the number of children is found positively correlated with the neuropathology of AD in several studies, while cumulative estrogen exposure calculated from the number of menstrual cycles is found associated with lower AD risk in another study. These studies suggest that estrogen levels, durations, and temporal patterns all matter for the final outcome. The protective effect of transient low-level estrogen during normal menstrual cycles does not necessarily mean that prolonged high-level estrogen exposure during pregnancy is beneficial. Most previous studies on this topic are focused on the immediate effects of low-level estrogen in the context of estrogen hormone replacement in the postmenopausal stage, while the enduring effects of high-level estrogen long after the cessation of the exposure are unclear. Few animal studies have examined how multiple pregnancies or pregnancy-associated high-level estrogen exposure affect late-life susceptibility to AD after the exposure is terminated. We intend to address this knowledge gap.