Elvis Cuevas, Ph.D.
Dr. Cuevas received a bachelor’s in pharmaco-biochemistry at the Meritorious Autonomous University of Puebla, Mexico and a doctorate in neurobiology from the Autonomous National University of Mexico (UNAM). Her graduate research focused on evaluation of the neuroprotection of flavonoids in a rodent model of Alzheimer’s disease (AD). Twice during her graduate studies, Dr. Cuevas was a guest worker for collaborative neuroscience projects between UNAM and NCTR. In 2010, she started a postdoctoral research position at NCTR with the main goal of evaluating the neurotoxic effects of cell phone radiation in both in vitro and in vivo models. In 2015, she received an appointment as a visiting scientist in NCTR’s Division of Neurotoxicology. Currently, she functions as an independent principal investigator within the division. The focal areas of Dr. Cuevas's current research at NCTR are in understanding the role gender plays in AD prevalence and the evaluation of specific neurotoxins on brain function. She has received funding for her work from the FDA’s Office of Women’s Health. Dr. Cuevas served as the president of the Arkansas Chapter of the Society for Neuroscience (2017-2018), where she actively participated in the annual outreach events of Brain Awareness week. She has received numerous travel awards and NCTR honor awards for her collaborative efforts and positive impact on center activities. She is an active participant in the Hispanic Organization of Toxicologists (HOT) and participates in the annual mentoring program, contributes communications in the HOT Toxenlaces newsletter, and presents webinars for the series “Updates in Toxicology,” developed by HOT in collaboration with Clubes de Ciencia México. Additionally, Dr. Cuevas has served as a reviewer for scientific publications in the field of neuroscience (Elsevier, Springer, and ScienceDirect).
Dr. Cuevas has been working to identify biomarkers—measurable indicators of the disease process—for specific neurodegenerative diseases. Identification of such biomarkers will contribute to the development of targeted therapies for neurodegenerative diseases and improve our knowledge about disease causation and prevention, possibly eliminating or reducing specific environmental factors that contribute to the development of Alzheimer’s and/or Parkinson diseases, with a special focus on the role of the blood-brain barrier (BBB). In addition to her work on neurodegenerative diseases, Dr. Cuevas is currently a co-investigator in projects evaluating the role that BBB dysfunction has on the neurochemical and neuropathological changes after 1) exposure to arsenic, drugs of abuse, and anesthetics, and 2) traumatic brain injury. Presently, she is evaluating sex differences in AD prevalence across different ethnicities and how the BBB might contribute to those differences, using a 3xTg AD mouse model, as well as the analysis of postmortem human tissues and fluids. These studies will aid in the development of new technologies/methodologies to improve and regulate the safety and efficacy of new drugs to slow disease progression in women and minority populations.
Professional Societies/National and International Groups
Arkansas Chapter of the Society for Neuroscience
2011 — Present
2017 — 2018
Association for Women in Science
2018 — Present
Hispanic Organization of Toxicologists (HOT)
2012 — 2017
International Drug Abuse Research Society
2011 — 2018
National System of Researchers (Mexico)
Member (Level I)
Society for Neuroscience
2004 — Present
Society of Toxicology
2011 — 2018
South Central Chapter of the Society of Toxicology
2012 — 2017
Downregulation of 14-3-3 Proteins in Alzheimer's Disease.
Gu Q., Cuevas E., Raymick J., Kanungo J., and Sarkar S.
Mol Neurobiol. 2020, 57: 32-40.
Impaired Amyloid Beta Clearance and Brain Microvascular Dysfunction are Present in the Tg-SwDI Mouse Model of Alzheimer's Disease.
Rosas-Hernandez H., Cuevas E., Raymick J.B., Robinson B.L., and Sarkar S.
Neuroscience. 2020, 440:48-55.
Characterization of Serum Exosomes from a Transgenic Mouse Model of Alzheimer's Disease.
Rosas-Hernandez H., Cuevas E., Raymick J.B., Robinson B.L., Ali S.F., Hanig J., and Sarkar S.
Curr Alzheimer Res. 2019, 16: 388-395.
Amyloid Beta 25-35 Induces Blood-Brain Barrier Disruption In Vitro.
Cuevas E., Rosas-Hernandez H., Burks S.M., Ramirez-Lee M.A., Guzman A., Imam S.Z., Ali S.F., and Sarkar S.
Metab Brain Dis. 2019, 34: 1365-1374.
Isolation and Culture of Brain Microvascular Endothelial Cells for In Vitro Blood-Brain Barrier Studies.
Rosas-Hernandez H., Cuevas E., Lantz S.M., Paule M.G., and Ali S.F.
Methods Mol Biol. 2018, 1727: 315-331.
Characterization of Biaxial Stretch as an In Vitro Model of Traumatic Brain Injury to the Blood-Brain Barrier.
Rosas-Hernandez H., Cuevas E., Escudero-Lourdes C., Lantz S.M., Gomez-Crisostomo N.P., Sturdivant N.M., Balachandran K., Imam S.Z., Slikker W., Jr., Paule M.G., and Ali S.F.
Mol Neurobiol. 2017, 55: 258-266.
Methamphetamine, 3,4-methylenedioxymethamphetamine (MDMA) and 3,4-methylenedioxypyrovalerone (MDPV) Induce Differential Cytotoxic Effects in Bovine Brain Microvessel Endothelial Cells.
Rosas-Hernandez H., Cuevas E., Lantz S.M., Rice K.C., Gannon B.M., Fantegrossi W.E., Gonzalez C., Paule M.G., and Ali S.F.
Neurosci Lett. 2016, 629: 125-130.
Protein Kinases and Parkinson's Disease.
Mehdi S.J., Rosas-Hernandez H., Cuevas E., Lantz S.M., Barger S.W., Sarkar S., Paule M.G., Ali S.F., and Imam S.Z.
Int J Mol Sci. 2016, 17: 1585.
Iron Oxide Nanoparticles Induce Dopaminergic Damage: In Vitro Pathways and In Vivo Imaging Reveals Mechanism of Neuronal Damage.
Imam S.Z., Lantz-McPeak S.M., Cuevas E., Rosas-Hernandez H., Liachenko S., Zhang Y., Sarkar S., Ramu J., Robinson B.L., Jones Y., Gough B., Paule M.G., Ali S.F., and Binienda Z.K.
Mol Neurobiol. 2015, 52: 913-926.
Modeling the Interaction between Quinolinate and the Receptor for Advanced Glycation End Products (RAGE): Relevance for Early Neuropathological Processes.
Serratos I.N., Castellanos P., Pastor N., Millan-Pacheco C., Rembao D., Perez-Montfort R., Cabrera N., Reyes-Espinosa F., Diaz-Garrido P., Lopez-Macay A., Martinez-Flores K., Lopez-Reyes A., Sanchez-Garcia A., Cuevas E., and Santamaria A.
PLoS One. 2015, 10: e0120221.
Developmental Toxicity Assay using High Content Screening of Zebrafish Embryos.
Lantz-McPeak S., Guo X., Cuevas E., Dumas M., Newport G.D., Ali S.F., Paule M.G., and Kanungo J.
J Appl Toxicol. 2015, 35: 261-272.
Ketamine Attenuates Cytochrome p450 Aromatase Gene Expression and Estradiol-17 beta Levels in Zebrafish Early Life Stages.
Trickler W.J., Guo X.Q., Cuevas E., Ali S.F., Paule M.G., and Kanungo J.
J Appl Toxicol. 2014, 34: 480-488.
Zebrafish Model in Drug Safety Assessment.
Kanungo J., Cuevas E., Ali S.F., and Paule M.G.
Curr Pharm Des. 2014, 20: 5416-5429.
Prolactin Protects Against the Methamphetamine-Induced Cerebral Vascular Toxicity.
Rosas-Hernandez H., Cuevas E., Lantz-McPeak S.M., Ali S.F., and Gonzalez C.
Curr Neurovasc Res. 2013, 10: 346-355.
Ketamine Induces Motor Neuron Toxicity and Alters Neurogenic and Proneural Gene Expression in Zebrafish.
Kanungo J., Cuevas E., Ali S.F., and Paule MG.
J Appl Toxicol. 2013, 33: 410-417.
Prolactin and Blood-Brain Barrier Permeability.
Rosas-Hernandez H., Cuevas E., Lantz S.M., Hamilton W.R., Ramirez-Lee M.A., Ali S.F., and Gonzalez C.
Curr Neurovasc Res. 2013, 10: 278-286.
Acetyl L-carnitine Protects Motor Neurons and Rohon-Beard Sensory Neurons Against Ketamine-Induced Neurotoxicity in Zebrafish Embryos.
Cuevas E., Trickler W.J., Guo X., Ali S.F., Paule M.G., and Kanungo J.
Neurotoxicol Teratol. 2013, 39: 69-76.
Nicotine Alters the Expression of Molecular Markers of Endocrine Disruption in Zebrafish.
Kanungo J., Cuevas E., Guo X.Q., Lopez A.G., Ramirez-Lee M.A., Trickler W., Paule M.G., and Ali S.F.
Neurosci Lett. 2012, 526: 133-137.
L-Carnitine Rescues Ketamine-Induced Attenuated Heart Rate and MAPK (ERK) Activity in Zebrafish Embryos.
Kanungo J., Cuevas E., Ali S.F., and Paule M.G.
Repro Toxicol. 2012, 33: 205-212.
On the In Vivo Early Toxic Properties of A-beta 25-35 Peptide in the Rat Hippocampus: Involvement of the Receptor-for-Advanced Glycation-End-Products and Changes in Gene Expression.
Cuevas E., Lantz S.M., Tobon-Velasco J.C., Newport G.D., Wu Q., Virmani A., Ali S.F., and Santamaria A.
Neurotoxicol Teratol. 2011, 33: 288-296.
Antioxidant Effects of Epicatechin on the Hippocampal Toxicity Caused by Amyloid-beta 25-35 in Rats.
Cuevas E., Limon D., Perez-Severiano F., Diaz A., Ortega L., Zenteno E., and Guevara J.
Eur. J. Pharmacol. 2009, 616: 122-127.
S-allylcysteine Prevents Amyloid-beta Peptide-Induced Oxidative Stress in Rat Hippocampus and Ameliorates Learning Deficits.
Perez-Severiano F., Salvatierra-Sanchez R., Rodriguez-Perez M., Cuevas-Martinez E.Y., Guevara J., Limon D., Maldonado P.D., Medina-Campos O.N., Pedraza-Chaverri J., and Santamaria A.
Eur. J. Pharmacol. 2004, 489: 197-202.
- Contact Information
- Elvis-Yane Cuevas-Martinez
ExpertiseApproachDomainTechnology & DisciplineNeurotoxicologyToxicology