Geraldine J. Kress, Ph.D.

Assistant Professor

Neurosciences Program

  • 314-362-5503



  • Alzheimer's Disease, Circadian System, Hippocampal Physiology, Neurodegeneration

  • circadian system influence on the limbic system during Alzheimer's disease pathogenesis and aging

Research Abstract:

We aim to understand how the circadian system influences limbic system functions such as memory performance during aging and Alzheimer’s disease (AD) progression. A growing body of evidence suggests that disruptions to the circadian system occur prior to the clinical onset of memory deficits in AD. Therefore, circadian function may be a modifiable risk factor for AD. We recently reported that the circadian system influences amyloid-β dynamics and pathology in a mouse model of AD (Kress et al., 2018 JEM). In my laboratory, we are extending this work to look in more detail as to how the circadian system may influence AD pathogenesis. This research program will identify pathophysiological changes, mechanisms, and possible strategies to ameliorate AD progression. Moreover, this research has the potential to provide important advances to our basic understanding for the role of circadian function during neurodegeneration. We use a combination of experimental approaches including in vivo / in vitro optogenetics and chemogenetics, chronic neural recordings, circadian and cognition behavior assays, and acute slice electrophysiology, as well as, protein and mRNA quantification and localization techniques. The lab is expanding and we are actively recruiting for graduate students and post-docs. There are several ongoing projects to work on depending on your interests and skill set. Contact me if you are interested in working on the circadian system and Alzheimer's disease pathogenesis.

Selected Publications:

Regulation of amyloid-β dynamics and pathology by the circadian clock.
Kress GJ, Liao F, Dimitry J, Cedeno MR, FitzGerald GA, Holtzman DM, Musiek ES.
J Exp Med. 2018 Apr 2;215(4):1059-1068. doi: 10.1084/jem.20172347.  

Mutant huntingtin enhances activation of dendritic Kv4 K+ channels in striatal spiny projection neurons. Carrillo-Reid L, Day M, Xie Z, Melendez AE, Kondapalli J, Plotkin JL, Wokosin DL, Chen Y, Kress GJ, Kaplitt M, Ilijic E, Guzman JN, Chan CS, Surmeier DJ. Elife. 2019 Apr 24;8:e40818. doi: 10.7554/eLife.40818. 

Fast phasic release properties of dopamine studied with a channel biosensor.
Kress GJ, Shu HJ, Yu A, Taylor A, Benz A, Harmon S, Mennerick S.
J Neurosci. 2014 Aug 27;34(35):11792-802. doi: 10.1523/JNEUROSCI.2355-14.2014. 

Impaired TrkB receptor signaling underlies corticostriatal dysfunction in Huntington's disease.
Plotkin JL, Day M, Peterson JD, Xie Z, Kress GJ, Rafalovich I, Kondapalli J, Gertler TS, Flajolet M, Greengard P, Stavarache M, Kaplitt MG, Rosinski J, Chan CS, Surmeier DJ.
Neuron. 2014 Jul 2;83(1):178-88. doi: 10.1016/j.neuron.2014.05.032. 

Convergent cortical innervation of striatal projection neurons.
Kress GJ, Yamawaki N, Wokosin DL, Wickersham IR, Shepherd GM, Surmeier DJ.
Nat Neurosci. 2013 Jun;16(6):665-7. doi: 10.1038/nn.3397. Epub 2013 May 12.
PMID: 23666180 Free PMC article.

Last Updated: 6/14/2021 1:09:42 PM

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