Legacy Research Institute

Laura Villasana, Ph.D.

Assistant Scientist
R.S. Dow Neuroscience Laboratories

CV (Updated December 2020)

Short Bio:

Dr. Villasana received her BS in Biology from the University of Houston and her Ph.D. in Behavioral Neuroscience from Oregon Health & Science University (OHSU) where she formed an interest in brain injury and recovery while studying the effects of cranial irradiation on cognitive function. During her post-doctoral training at the Vollum Institue and the Department of Anesthesiology & Perioperative Medicine (APOM) at OHSU, she expanded on her developing interest in neurogenesis. With support from an NRSA she and her mentors confirmed that the new neurons generated in response to TBI functionally integrate within the hippocampus and discovered that post-traumatic neurogenesis is modulated by clinically relevant sedatives. She then accepted an Assistant Professorship within the APOM department at OHSU where she established a research program to better understand the functional significance of new neurons on memory recovery after TBI. During this time she also accepted a position as the Director of the Behavioral Core where she formed collaborations with other scientist to examine recovery following various forms of brain injury.

Dr. Villasana joined LRI in 2020 where she continues to advance her research in determining how the generation of new neurons after injury can be fostered to help improve cognitive recovery.

Publication Highlights:

Diazepam inhibits post-traumatic neurogenesis and blocks aberrant dendritic development.
Villasana, L.E., Peters, A., McCallum, R., Liu, C., and Schnell, E.
J. Neurotraum. (2019) 36(16): 2454-2467 PMID 30794026
https://pubmed.ncbi.nlm.nih.gov/30794026/

Ketamine alters hippocampal cell proliferation and improves learning in mice after traumatic brain injury.
Peters, A., Villasana, L.E, and Schnell, E.
Anesthesiology (2018) 129(2): 278-295. PMID 29734230
https://pubmed.ncbi.nlm.nih.gov/29734230/

Functional integration of adult-born neurons after traumatic brain injury.
Villasana, L.E., Kim, K.N., Westbrook, G.L. and Schnell, E.
eNeuro (2015) 2(5): 1-17. PMID 26478908
https://pubmed.ncbi.nlm.nih.gov/26478908/

Neurologic impairment following experimental closed head injury predicts post-traumatic neurogenesis.
Villasana, L.E., Westbrook, G. and Schnell, E.
Exp Neurol. (2014) 261:156-62. PMID 24861442
https://pubmed.ncbi.nlm.nih.gov/24861442/

Research Interests:

• Post-traumatic neurogenesis in hippocampal function after traumatic brain injury
• Modulation of neurogenesis after traumatic brain injury
• Long-term effects of traumatic brain injury on neural stem cells & neurogenesis

Research Focus:

One of the main focus of my research is to determine what type of contribution new neurons born after traumatic brain injury (TBI) make to their network- that is, whether they help or hinder information processing within the hippocampus, a brain region critical for memory. Because new neurons in the adult hippocampus are important for certain types of memory, it is believed that increases in neurogenesis in response to TBI represents an adaptive mechanism contributing to hippocampal recovery. However the neurons born after TBI are not the same as those born in a non-injured brain; they migrate to regions not normally observed in a non-injured brain and have abnormal dendrites. My lab uses genetic, pharmacologic and behavioral approaches in mice to determine whether increases in neurogenesis after TBI helps or hinders hippocampal function.

We are also interested in determining whether normalizing the aberrant development of neurons born after TBI facilitates memory recovery. Results from this research is applicable to other injuries and diseases such as stroke and Alzheimer’s Disease where new neurons in the adult brain are also abnormal.

In contrast to robust increases in neurogenesis acutely after TBI, neurogenesis drops below normal levels months after TBI, likely due to neural stem cell exhaustion. My lab is examining the response of the neural stem cells to TBI and determining whether clinically feasible interventions can mitigate this deficit and improve long-term cognitive outcomes.

Memory dysfunction is one of the most common and long-lasting complications following TBI. Given that new neurons play important roles in memory, and that their increase in response to TBI naturally occurs, post-traumatic neurogenesis holds great therapeutic promise in facilitating short- and long-term memory recovery. The knowledge gained from our studies will allow the field to move forward in determining how to modulate neurogenesis to fully benefit from its therapeutic potential.