Claudia R. Rangel-Barajas, PhD
Assistant Research Professor of Medical & Molecular Genetics
- Address
-
NB 108A
MMGE
Indianapolis, IN
Bio
Dr. Claudia Rangel-Barajas holds a Master of Science in Pharmacology and a Ph.D. in Neuropharmacology from the Center for Research and Advanced Studies of the National Polytechnic Institute in Mexico City. Her research primarily focuses on the neurosciences, with a particular emphasis on neurodegeneration. She has published extensively in leading scientific journals and presented her work at numerous national and international conferences.
Dr. Rangel-Barajas currently serves as the Project Manager for the MODEL-AD consortium at the Stark Neurosciences Research Institute, Indiana University School of Medicine. Funded by the National Institute on Aging, MODEL-AD is a collaborative effort involving prominent institutions such as The Jackson Laboratory, Sage Bionetworks, the University of California, Irvine, and the University of Pittsburgh School of Medicine. In her role, Dr. Rangel-Barajas leads efforts to standardize and optimize the development of Alzheimer’s disease (AD) animal models. The MODEL-AD Center is pioneering the creation of next-generation in vivo AD models based on human data, establishing rigorous protocols for their characterization. These models are designed to closely mirror the pathophysiological features of AD, ensuring that they are valuable tools for preclinical drug development and enabling rapid dissemination of validated models, protocols, and data across the research community.
In addition to her work with MODEL-AD, Dr. Rangel-Barajas holds the position of Research Assistant Professor at Indiana University School of Medicine. She is also a key collaborator with the Target Enablement to Accelerate Therapy Development for Alzheimer’s Disease (TREAT-AD) drug discovery center, which aims to overcome the challenges of discovering new therapeutic targets and accelerating the development of promising treatments for Alzheimer’s disease.
Key Publications
Rangel-Barajas C and Rebec GV. Dysregulation of corticostriatal connectivity in Huntington's disease: A Role for Dopamine Modulation. J. of Huntington’s Disease, 2016, 5;5(4):303-331
Ponzi A, Barton SJ, Bunner KD, Rangel-Barajas C, Zhang ES, Miller BR, Rebec GV, Kozloski J. Striatal network modeling in Huntington's Disease. PLoS Comput Biol. 2020 Apr 17;16(4):e1007648. doi: 10.1371/journal.pcbi.1007648.
Rangel-Barajas C, Boehm II SL, Logrip ML. Altered Excitatory transmission in striatal neurons after chronic etanol consumption in selectively bred crossed high alcohol-preferring mice. Neuropharmacology 190 (2021) 33857521.
Vishakh Iyer, Claudia Rangel-Barajas, Taylor J Woodward, Abhijit Kulkarni, Lucas Cantwell, Jonathon D Crystal, Ken Mackie, George V Rebec, Ganesh A Thakur, Andrea G Hohmann. Negative allosteric modulation of CB1 cannabinoid receptor signaling suppresses opioid-mediated reward. Pharmacol Res. 2022 Sep 28;185:106474.
Emma Woodward, Claudia Rangel-Barajas*, Amanda Ringland, Marian L. Logrip, Laurence Coutellier. Sex-specific timelines for adaptations of prefrontal parvalbumin neurons in response to stress and changes in anxiety- and depressive-like behaviors. eNeuro, 2023; 10(3); 1-19. ENEURO0300-22.2223 (*Equal contribution)
Kotredes KP, Pandey RS, Persohn S, Elderidge K, Burton CP, Miner EW, Haynes KA, Santos DFS, Williams SP, Heaton N, Ingraham CM, Lloyd C, Garceau D, O'Rourke R, Herrick S, Rangel-Barajas C, Maharjan S, Wang N, Sasner M, Lamb BT, Territo PR, Sukoff Rizzo SJ, Carter GW, Howell GR, Oblak AL. Characterizing molecular and synaptic signatures in mouse models of late-onset Alzheimer's disease independent of amyloid and tau pathology. Alzheimer’s Dement. 2024 Jun;20(6):4126-4146. doi: 10.1002/alz.13828. Epub 2024 May 12. PMID: 38735056; PMCID: PMC11180851.
| Year | Degree | Institution |
|---|---|---|
| 2010 | PhD | Cinvestav IPN |
| 2005 | MS | Cinvestav IPN |
| 2002 | BS | National Autonomous University of Mexico |
My research interests include neurotransmitter systems, neural connectivity, and neurodegeneration. Early in my career, I studied altered basal ganglia connectivity, which is crucial for cognition, learning, and action control. I have also explored neuronal receptor pharmacology, dysregulated signaling pathways, and changes in neuronal excitability linked to neurodegenerative diseases, revealing common mechanisms across these conditions.
Currently, I am working to identify new therapeutic targets related to neuroinflammation to support preclinical drug development for AD. Additionally, my research has examined how biological and environmental factors influence synaptic strength and behavior, particularly the shift from action selection to habitual behavior. Using in vivo electrophysiology and ex vivo patch-clamp techniques, I have investigated synaptic adaptations in glutamatergic and GABAergic neurons, and how glutamate-dopamine interactions in the basal ganglia contribute to maladaptive behaviors, including those linked to substance abuse, anxiety, and sex differences.