Paul Shaw, PhD

Paul Shaw, PhD

Professor of Neuroscience

Shaw Lab | Google Scholar Profile


Despite the fact that sleep is conserved throughout the animal kingdom, the function of sleep remains one of the last major unsolved biological mysteries facing neuroscience today. Human, rodent and fly studies clearly demonstrate that sleep plays an important role in memory consolidation. However, recent human studies reveal that sleep plays a much more intricate role in brain functioning than simply stabilizing and consolidating memories. Indeed, sleep is vital for the off-line processing of information including improving creative thinking and promoting the discovery of creative insights: An historical example is the discovery of the structure of the benzene ring during a dream.

The Shaw laboratory uses the genetic model organism Drosophila melanogaster to elucidate the molecular mechanisms linking sleep to neuronal plasticity. The lab has demonstrated that we can fully restore cognitive functioning to a diverse set of classic memory mutants simply by enhancing their sleep. In these experiments, sleep was able to reverse cognitive deficits without restoring the causal molecular lesion or structural defect. In addition sleep reversed cognitive deficits in two separate models of Alzheimer’s disease.

Current studies are focused on the molecular mechanism that allows sleep to initiate such an extreme form of neuronal plasticity that allows sleep to reverse cognitive deficits even when they are caused by catastrophic genetic and structural lesions.

Selected publications

  • Melnattur K, Shaw P. Staying awake to stay alive: A circuit controlling starvation-induced waking. PLoS Biology. 2019; 17(3)e3000199.
  • Dissel S, Angadi V, Kirszenblat L, Suzuki Y, Donlea J, Klose M, Koch Z, English D, Winsky-Sommerer R, van Swinderen B, et al. Sleep restores behavioral plasticity to Drosophila mutants. Curr Biol. May 18, 2015; 25(10):1270-81.
  • Dissel S, Seugnet L, Thimgan MS, Silverman N, Angadi V, Thacher PV, Burnham MM, Shaw PJ. Differential activation of immune factors in neurons and glia contribute to individual differences in resilience/vulnerability to sleep disruption. Brain, Behavior, and Immunity. 2014; 47:75–85.
  • Donlea JM, Leahy A, Thimgan MS, Suzuki Y, Hughson BN, Sokolowski MB, Shaw PJ. Foraging alters resilience/vulnerability to sleep disruption and starvation in Drosophila. Proc Natl Acad Sci U S A. 2012 Feb 14; 109(7):2613-8. Epub 2012 Jan 30.
  • Donlea JM, Thimgan MS, Suzuki Y, Gottschalk L, Shaw PJ. Inducing sleep by remote control facilitates memory consolidation in Drosophila. Science. 2011; 322:1571-1576.
  • Donlea JM, Ramanan N, Shaw PJ. Use-dependent plasticity in clock neurons regulates sleep need in Drosophila. Science. 2009; 324: 105-108.
  • Seugnet L, Galvin JE, Suzuki Y, Gottschalk L, Shaw PJ. Persistent short-term memory defects following sleep deprivation in a Drosophila Model of Parkinson’s disease. Sleep. 2009; 32(8):984-992.
  • Seugnet L, SuzukiY, Vine L, Gottschalk L, Shaw PJ. D1 Receptor activation in the mushroom bodies rescues sleep-loss-induced learning impairments in Drosophila. Curr Biol. 2008 Aug 5; 18(15):1110-7.
  • Ganguly-Fitzgerald I, Donlea J, Shaw PJ. Waking experience affects sleep need in Drosophila. Science. 2006; 313:1775-1781.


1985 BA, Psychology & Criminal Justice, Niagara University

1990 MA, Psychology, San Jose State University

1996 PhD, Biopsychology, University of Chicago