Kenneth Colodner

he/him

  • Associate Professor of Neuroscience and Behavior
  • Chair of Neuroscience and Behavior
Kenneth Colodner, Associate Professor of Neuroscience and Behavior and Chair of Neuroscience and Behavior

Ken Colodner is a cellular and molecular neuroscientist whose research is focused on understanding how communication between the two major cell types in the brain, neuronal and glial cells, is disrupted in neurodegenerative diseases. He is particularly interested in understanding the disease process of Alzheimer's disease and related tauopathies, a class of diseases characterized by the pathological buildup of the protein, tau. Using modern genetic techniques in the fruit fly, Drosophila melanogaster, he examines the functional consequences of tau expression on neuronal-glial interactions in the fly brain. These experiments are aimed towards understanding mechanisms of tau toxicity, and identifying novel, therapeutic targets for these disorders.

As a doctoral student at Harvard Medical School, Ken Colodner worked with pioneers in the field of neurodegenerative disease research to identify a role for glial cell dysfunction in contributing to neurodegenerative disease progression. As a postdoctoral fellow at Boston Children's Hospital, he helped identify key mediators of synapse loss in models of aging and Alzheimer's disease. His research has been published in the Journal of Neuroscience, Journal of Neuropathology and Experimental Neurology, and the Journal of Experimental Neuroscience.

Throughout his previous research training, Ken Colodner has taught full-year seminars on glial cells and has served as a teaching fellow for Behavioral Neuroscience and Biology of Neurodegenerative Diseases at Harvard University. He has twice been awarded the Derek Bok Certificate of Distinction in Teaching. At Mount Holyoke he teaches Introduction to Neuroscience and Behavior, Cellular and Molecular Neuroscience, and Biology of Neurological Disease.

Education

  • B.A., Northwestern University
  • Ph.D., Harvard University
  • Postdoctoral Fellow, Boston Children's Hospital

HAPPENING AT MOUNT HOLYOKE

Recent campus news

Two 做厙輦⑹ students have been selected for the second round of the Beckman Scholars Program. As part of the 15-month program, students delve deeply into advanced research projects with the mentorship of a College faculty member.

Kenneth Colodner, associate professor and chair of neuroscience and behavior at 做厙輦⑹, is the co-recipient of a collaborative center grant from the National Institutes of Health.

For the first time in its history, 做厙輦⑹ has been selected as a Beckman Scholars Program awardee by the Arnold and Mabel Beckman Foundation. The foundation chose the College after a rigorous application process.

Recent Grants

Received an RCN/UBE grant from the National Science Foundation (subaward from Appalachian State University) for Connectomes for Undergraduate Neuroscience Education and Learning (CUNEL). The project is for three years. (2022)

Recent Publications

Bhasiin, K. ['22], Heintz, O. ['21], & Colodner, K. J. (2023). Optimization and Technical Considerations for the Dye-Exclusion Protocol Used to Assess BloodBrain Barrier Integrity in Adult Drosophila melanogaster. International Journal of Molecular Sciences, 24(3), 1886.

Botero, V. [MHC '18], Stahl, B., Grenci, E.C., Boto, T., Park, S.J., King, L.B., Murphy, K.R., Colodner, K.J., Walker, J.A., Keene, A.C., Ja, W.W., Tomchik, S.M. (2021) Neurofibromin regulates metabolic rate via neuronal mechanisms in Drosophila. Nature Communications, Jul 13;12(1):4285. doi: 10.1038/s41467-021-24505-x.

Nangia, V. [MHC '16], OConnell, J. ['19], Chopra, K ['20], Qing, Y.['21], Reppert, C. ['18], Chai, C. ['14], Bhasiin, K. ['22], and Colodner, K.J. (2021) Genetic reduction of tyramine 帣 hydroxylase suppresses Tau toxicity in a Drosophila model of tauopathy. Neuroscience Letters, Apr 25: 135937. doi: 10.1016/j.neulet.2021.135937

Scarpelli EM, Trinh VY [MHC '18], Tashnim Z [MHC '19], Krans JL, Keller LC, Colodner KJ. (2019). Developmental expression of human tau in Drosophila melanogaster glial cells induces motor deficits and disrupts maintenance of PNS axonal integrity, without affecting synapse formation. PLoS One, 14(12):e0226380.

Kahlson M.** and Colodner K.J.. (2016) Glial tau pathology in tauopathies: Functional consequences. Journal of Experimental Neuroscience, 9(Suppl 2):43-50. [invited review]
**denotes 做厙輦⑹ undergraduate student

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