Center Director, Center for Neuroscience
Thomas Kilduff, Ph.D., is an expert in the neurobiology of sleep and wakefulness, sleep disorders, and the biological clock. Kilduff was co-first author on the paper that originally described hypocretin/orexin (Hcrt), a neuropeptide system that stimulates arousal and is involved in wakefulness regulation. Dysfunction of the Hcrt system results in narcolepsy, a sleep disorder characterized by excessive daytime sleepiness and a sudden loss of muscle tone known as cataplexy.
In addition to basic research on sleep, his group conducts in vitro and in vivo pharmacology studies related to the development of new medications for the treatment of sleep disorders. Government agencies, private foundations, and pharmaceutical companies have supported this research. Kilduff has authored or co-authored more than 200 published abstracts, scientific articles, and book chapters.
Kilduff was previously a senior research scientist at Stanford University’s Center for Sleep and Circadian Neurobiology. He has been elected to the board of directors of the Sleep Research Society (SRS) and served as secretary/treasurer for both the SRS and SRS Foundation. He received his Ph.D. in biological sciences from Stanford University. In 2010, Kilduff was named a Fellow of the American Association for the Advancement of Science (AAAS).
Kilduff was named an SRI Fellow in 2010 and a Distinguished Scientist by the SRS in 2017.
Recent publicationsmore +
In the present study, we systematically evaluated the efficacy of two NOPR agonists, Ro64-6198 and SR16835, on sleep/wake in rats, mice, and Cynomolgus macaques.
Evaluation of the efficacy of the hypocretin/orexin receptor agonists TAK-925 and ARN-776 in narcoleptic orexin/tTA; TetO-DTA mice
We evaluated the efficacy of two small molecule hypocretin/orexin receptor-2 (HCRTR2) agonists in narcoleptic male orexin/tTA; TetO-DTA mice.
The development of sleep/wake disruption and cataplexy as hypocretin/orexin neurons degenerate in male vs. female Orexin/tTA; TetO-DTA Mice
We compared the development of narcoleptic symptomatology in male vs. female orexin-tTA; TetO-DTA mice, a model in which Hcrt neuron degeneration can be initiated by removal of doxycycline (DOX) from the diet.
Whether the cause of daytime sleepiness in narcolepsy type 1 (NT1) is a direct consequence of the loss of orexin (ORX) neurons or whether low orexin reduces the efficacy of the monoaminergic systems to promote wakefulness is unclear.
Animal models have advanced not only our understanding of the etiology and phenotype of the sleep disorder narcolepsy but have also informed sleep/wake regulation more generally.
The involvement of this system in a disorder characterized by the loss of control over arousal state boundaries also suggested its role as a critical component of endogenous sleep-wake regulatory circuitry.