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Ana G Cristancho, MD, PhD
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Assistant Professor of Neurology
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Department: Neurology
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Graduate Group Affiliations
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- Cell and Molecular Biology 64
- Neuroscience 6a
- Pharmacology e
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Contact information
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Colket Translational Research Building, 6020
39 3501 Civic Center Blvd
Philadelphia, PA 19104
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39 3501 Civic Center Blvd
Philadelphia, PA 19104
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Education:
21 7 BS 23 (Biology and Philosophy) c
2c University of Miami, 2004.
21 8 PhD 27 (Cell and Molecular Biology) c
33 University of Pennsylvania, 2011.
21 7 MD c
33 University of Pennsylvania, 2013.
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Permanent link21 7 BS 23 (Biology and Philosophy) c
2c University of Miami, 2004.
21 8 PhD 27 (Cell and Molecular Biology) c
33 University of Pennsylvania, 2011.
21 7 MD c
33 University of Pennsylvania, 2013.
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16a The Cristancho lab is interested in understanding the epigenetic mechanisms driving long-term neurodevelopmental disabilities from acquired prenatal and perinatal brain injury. We posit that even in the setting of little cell death, epigenome disruption during critical stages of early brain development persistently alters brain maturation and function.
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11 Keywords:
77 prenatal brain injury, epigenetics, neurodevelopmental disorders, multi-omics, behavior, translational, hypoxia
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19 Research Details:
202 Prenatal and perinatal brain injuries, including prenatal hypoxia, are among the most common causes of neurodevelopmental disabilities worldwide, ranging from developmental delays, autism, epilepsy, cerebral palsy, and learning disabilities. However, despite their prevalence, we have almost no directed therapies for these disorders. Part of the challenge is that these injuries are variable in what causes them, how long the insult lasts, and lead to a wide variety of disabilities in affected children.
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1fc To study these questions, we use a combination of animal and cell culture models and take advantage of multi-omic approaches to garner a multi-dimensional understanding of these complex brain injuries on different cell types. We then use physiologic, behavioral, and imaging outputs to link changes in the epigenetic signature to functional outcomes to determine which changes to the epigenome are important for modulating the severity of neurodevelopmental deficits after developmental brain injury.
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1a7 We are currently focusing on a model of transient prenatal hypoxia, where we found there is little early cell death, but there are persistent deficits in adult animals (decreased seizure threshold and other behavior anomalies). Using single nucleus RNA-seq and ATAC-seq, we are currently unraveling the cell type-specific dynamics that drive these persistent functional deficits long after the insult has occurred.
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1a Rotation Projects:
48 Please contact us for a discussion of possible rotation projects.
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Description of Clinical Expertise
2c Fetal and Neonatal Neurology71
Description of Research Expertise
24 Research Interests:16a The Cristancho lab is interested in understanding the epigenetic mechanisms driving long-term neurodevelopmental disabilities from acquired prenatal and perinatal brain injury. We posit that even in the setting of little cell death, epigenome disruption during critical stages of early brain development persistently alters brain maturation and function.
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11 Keywords:
77 prenatal brain injury, epigenetics, neurodevelopmental disorders, multi-omics, behavior, translational, hypoxia
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19 Research Details:
202 Prenatal and perinatal brain injuries, including prenatal hypoxia, are among the most common causes of neurodevelopmental disabilities worldwide, ranging from developmental delays, autism, epilepsy, cerebral palsy, and learning disabilities. However, despite their prevalence, we have almost no directed therapies for these disorders. Part of the challenge is that these injuries are variable in what causes them, how long the insult lasts, and lead to a wide variety of disabilities in affected children.
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1fc To study these questions, we use a combination of animal and cell culture models and take advantage of multi-omic approaches to garner a multi-dimensional understanding of these complex brain injuries on different cell types. We then use physiologic, behavioral, and imaging outputs to link changes in the epigenetic signature to functional outcomes to determine which changes to the epigenome are important for modulating the severity of neurodevelopmental deficits after developmental brain injury.
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1a7 We are currently focusing on a model of transient prenatal hypoxia, where we found there is little early cell death, but there are persistent deficits in adult animals (decreased seizure threshold and other behavior anomalies). Using single nucleus RNA-seq and ATAC-seq, we are currently unraveling the cell type-specific dynamics that drive these persistent functional deficits long after the insult has occurred.
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1a Rotation Projects:
48 Please contact us for a discussion of possible rotation projects.
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176 DaSilva S*, Cassidy M*, Gadra E, Smith M, Ahrens-Nicklas R, Cristancho AG. *equal contributing authors: Persistent brain mitochondrial dysfunction after mild transient prenatal hypoxia as a potential therapeutic target beyond the neonatal period. International Newborn Brain Conference February 2026.
163 Scher MS, Adalat S, Eyre HA, Msall M, Ramey S, Ramey CT, Cristancho AG, Markvarde A.: Transdisciplinary fetal-neonatal neurology training integrates women's and children's health with life-course brain capital strategies: a narrative review. Frontiers in Neurology (accepted) 2026.
13d Anton L*, Cristancho AG*, Ferguson B, Shin S, Ravel J, Elovitz MA. *Equally contributing authors: Cervicovaginal microbiome alters transcriptomic and epigenomic signatures across cervicovaginal epithelial barriers. Microbiome November 2025.
117 Cristancho AG, Joseph D, Chauhan PS, Gadra E, Gadra EC, Zarrinnegar D, Rodriguez B, Marsh ED : Chromatin Disruption After Prenatal Hypoxia Predicts Lasting Neuron Deficits. bioRxiv (preprint) November 2025.
140 Chauhan PS, Rodriguez B, Nova C, Smith M,Gadra E, Cristancho AG : Unraveling the Impact of Prenatal insult on Neural Stem Cell Behavior: Implication for Neurodevelopmental Disorders. American Neurological Association Annual Meeting September 2025.
1a1 DaSilva S*, Cassidy M*, Gadra E, Smith M, Ahrens-Nicklas R, Cristancho AG. *equal contributing authors: Potential For Early Variance of Citric Acid Cycle Metabolites Contributing to Lasting Mitochondrial and Epigenetic Disruption After Prenatal Hypoxia In Glutamatergic Neurons. American Neurological Association Annual Meeting September 2025.
a6 Jacobwitz M, Xie M, Catalano J, Helbig I, Gaynor JW, Burnham N, Linn RL, Gebb J, Russell MW, Chaiyachati BH, Cristancho AG d8 : DNA Methylation Differences Stratified by Normalized Fetal/Placental Weight Ratios Suggest Neurodevelopmental Deficits in Neonates with Congenital Heart Disease. PLOS ONE August 2025.
18e Rashid R, Bach A, Patel V, Saha K, Gebb J, Soni S, Miller K, Schindewolf E, Cristancho AG, Agarwal S : Agenesis of the corpus callosum: clinical characteristics and outcomes among children with complete or partial agenesis in a twenty-year retrospective cohort. Journal of Child Neurology Page: 8830738251345652, June 2025.
65 Cassidy MM, Yudkoff M, Ahrens-Nicklas RC*, Cristancho AG* 2 e5 : Branched Chain Amino Acid Metabolism in Developmental Brain Injury: Putative Mechanisms and Therapeutic Potential. Developmental Neuroscience 11: 1-15, March 2025 Notes: *Co-corresponding authors.
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Selected Publications
14e Porcari, G, Rashid R, Mulvihill C, Beslow LA, Dubbs H, Schindewolf E, Gebb J, Agarwal S, Whitehead MT, Cristancho AG. : Stratification of Phenotypes in Childhood-Onset COL4A1/COL4A2–Related Disorders Based on Age of Presentation. Neurology Genetics June 2026.176 DaSilva S*, Cassidy M*, Gadra E, Smith M, Ahrens-Nicklas R, Cristancho AG. *equal contributing authors: Persistent brain mitochondrial dysfunction after mild transient prenatal hypoxia as a potential therapeutic target beyond the neonatal period. International Newborn Brain Conference February 2026.
163 Scher MS, Adalat S, Eyre HA, Msall M, Ramey S, Ramey CT, Cristancho AG, Markvarde A.: Transdisciplinary fetal-neonatal neurology training integrates women's and children's health with life-course brain capital strategies: a narrative review. Frontiers in Neurology (accepted) 2026.
13d Anton L*, Cristancho AG*, Ferguson B, Shin S, Ravel J, Elovitz MA. *Equally contributing authors: Cervicovaginal microbiome alters transcriptomic and epigenomic signatures across cervicovaginal epithelial barriers. Microbiome November 2025.
117 Cristancho AG, Joseph D, Chauhan PS, Gadra E, Gadra EC, Zarrinnegar D, Rodriguez B, Marsh ED : Chromatin Disruption After Prenatal Hypoxia Predicts Lasting Neuron Deficits. bioRxiv (preprint) November 2025.
140 Chauhan PS, Rodriguez B, Nova C, Smith M,Gadra E, Cristancho AG : Unraveling the Impact of Prenatal insult on Neural Stem Cell Behavior: Implication for Neurodevelopmental Disorders. American Neurological Association Annual Meeting September 2025.
1a1 DaSilva S*, Cassidy M*, Gadra E, Smith M, Ahrens-Nicklas R, Cristancho AG. *equal contributing authors: Potential For Early Variance of Citric Acid Cycle Metabolites Contributing to Lasting Mitochondrial and Epigenetic Disruption After Prenatal Hypoxia In Glutamatergic Neurons. American Neurological Association Annual Meeting September 2025.
a6 Jacobwitz M, Xie M, Catalano J, Helbig I, Gaynor JW, Burnham N, Linn RL, Gebb J, Russell MW, Chaiyachati BH, Cristancho AG d8 : DNA Methylation Differences Stratified by Normalized Fetal/Placental Weight Ratios Suggest Neurodevelopmental Deficits in Neonates with Congenital Heart Disease. PLOS ONE August 2025.
18e Rashid R, Bach A, Patel V, Saha K, Gebb J, Soni S, Miller K, Schindewolf E, Cristancho AG, Agarwal S : Agenesis of the corpus callosum: clinical characteristics and outcomes among children with complete or partial agenesis in a twenty-year retrospective cohort. Journal of Child Neurology Page: 8830738251345652, June 2025.
65 Cassidy MM, Yudkoff M, Ahrens-Nicklas RC*, Cristancho AG* 2 e5 : Branched Chain Amino Acid Metabolism in Developmental Brain Injury: Putative Mechanisms and Therapeutic Potential. Developmental Neuroscience 11: 1-15, March 2025 Notes: *Co-corresponding authors.
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