Fabian Fernandez

Fabian Fernandez

Assistant Professor, Psychology
Assistant Professor, Evelyn F Mcknight Brain Institute
Assistant Professor, Neurology
Assistant Professor, Neuroscience - GIDP
Assistant Professor, BIO5 Institute
Primary Department
Department Affiliations
Contact
(520) 621-7447

Work Summary

Fabian-Xosé Fernandez's work includes a focus on parsing the logic used by the circadian pacemaker to interpret multidimensional light patterns, developing light-emitting diode (LED) photo-stimulation protocols to improve mental and physical health across the lifespan, and understanding the role that nocturnal wakefulness plays in suicide risk and developing countermeasures centered around light exposure.

Research Interest

Fabian-Xosé Fernandez, PhD, Departments of Psychology and Neurology, McKnight Brain InstituteCircadian timekeeping is fundamental to human health. Unfortunately, under many clinical circumstances, the temporal organization of our minds and bodies can stray slowly from the Universal Time (UT) that is set with the Earth’s rotation. This disorganization has been linked to progression of several age-related and psychiatric diseases. Non-invasive phototherapy has the potential to improve disease outcomes, but the information that the brain’s clock tracks in twilight (or any electric light signal) to assure that a person entrains their sleep-wake cycles to the outside world is not understood. The central theme of my research program is to fill in this blank and to usher in an era where therapeutically relevant “high-precision” light administration protocols are institutionalized at the level of the American Medical and Psychiatric Associations to change the standard of care for a wide variety of conditions that impair quality of life. Of the conditions my lab is currently studying, we are particularly interested in how chronic and quick, sequenced light exposure can be designed to: 1. promote normal healthy aging and 2. strengthen adaptive cognitive/emotional responses to being awake in the middle of the night (12-6AM), a key interval of the 24-h cycle that we have associated with increased suicidal ideation and mortality. Our circadian work on suicide is done in very close partnership with the University of Arizona Sleep Health and Research Program directed by Dr. Michael A. Grandner.

Publications

Fernandez, F., Trinidad, J. C., Blank, M., Feng, D., Burlingame, A. L., & Garner, C. C. (2009). Normal protein composition of synapses in Ts65Dn mice: a mouse model of Down syndrome. Journal of neurochemistry, 110(1), 157-69.

Down syndrome (DS) is the most prevalent form of intellectual disability caused by the triplication of approximately 230 genes on chromosome 21. Recent data in Ts65Dn mice, the foremost mouse model of DS, strongly suggest that cognitive impairment in individuals with DS is a consequence of reduced synaptic plasticity because of chronic over-inhibition. It remains unclear however whether changes in plasticity are tied to global molecular changes at synapses, or are due to regional changes in the functional properties of synaptic circuits. One interesting framework for evaluating the activity state of the DS brain comes from in vitro studies showing that chronic pharmacological silencing of neuronal excitability orchestrates stereotyped changes in the protein composition of synaptic junctions. In the present study, we use proteomic strategies to evaluate whether synapses from the Ts65Dn cerebrum carry signatures characteristic of inactive cortical neurons. Our data reveal that synaptic junctions do not exhibit overt alterations in protein composition. Only modest changes in the levels of synaptic proteins and in their phosphorylation are observed. This suggests that subtle changes in the functional properties of specific synaptic circuits rather than large-scale homeostatic shifts in the expression of synaptic molecules contribute to cognitive impairment in people with DS.