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Auerbach Lab

David S. Auerbach, Ph.D.David Auerbach

Assistant Professor, Department of Medicine, Aab Cardiovascular Research Institute (CVRI) - Primary

Department of Pharmacology & Physiology - Secondary

2011 | Ph.D. | Pharmacology | SUNY Upstate Medical University, Syracuse NY

2004 | M.S. | Physiology & Biophysics | Case Western Reserve University, Cleveland, OH

Auerbach Profile

Research Overview

We are a translational research group that utilize cellular, animal, and patient database approaches to investigate the co-prevalence, risk, and mechanisms for neuro-cardiac electrical disturbances and Sudden Unexpected Death in Epilepsy (SUDEP.)

Research Projects

Project 1: Electrical Disturbances in the Brain & Heart in Long QT Syndrome – Dangerous Combination

 Figure 1Patients with genetic ion channel diseases develop electrical disturbances in the brain (seizures) and heart (arrhythmias) that can lead to sudden death. Our lab takes a multi-system approach to explore the implications of genetic ion channel diseases on neuro-cardiac electrical function. For example, in severe genetic forms of epilepsy, in addition to seizures, there are alterations in cardiac electrical function, cardiac arrhythmias, and sudden death (Auerbach DS et al. 2013.)

Next, approaching these neuro-cardiac investigations in the opposite direction, we are assessing the co-prevalence and severity of seizures and cardiac arrhythmias in a classically studied cardiac disease, called Long QT Syndrome (LQTS, Auerbach et al. 2016.) LQTS is a genetic disease, characterized by cardiac electrocardiographic (ECG) pathologies, arrhythmias, and a high risk of sudden death. Mutated genes in LQTS1-3 are expressed in the heart and brain, and anti-seizure drugs alter the risk of arrhythmias in LQTS patients (Auerbach et al. 2018.)Using both LQTS patient registries and animal/cellular models of LQTS we are exploring the mechanisms for this dual system disease, and the potential intricate crosstalk between the brain and heart. 

The LQTS registry provides a unique and powerful resource to advance LQTS and epilepsy research. The Rochester-based LQTS Registry is the largest (>18,000 subjects) and most deeply annotated LQTS database in the world. It contains detailed clinical and genetic information from LQTS patients, plus affected and unaffected family members. Using cellular and animal models of LQTS, plus state of the art in vivo/in vitro techniques (e.g., radiotelemetry ECGs & single cell electrophysiology), we are examining the direct vs. indirect mechanisms for the neuro-cardiac disease manifestations and progression.

Project 2: Cardiac and Autonomic Abnormalities in Patients at Risk for SUDEPFigure 2

Millions of Americans have epilepsy. They have a 24-fold higher risk of sudden death. Unfortunately, the cause of death is often unknown and termed Sudden Unexpected Death in Epilepsy (SUDEP). Thus, we are unable to predict a person’s risk of SUDEP. Cardiac events are one mechanism for SUDEP. Cardiac ECG abnormalities and arrhythmias are reported surrounding seizures and preceding SUDEP. Also, many genetic forms of epilepsy, especially SUDEP cases, are associated with mutations in genes expressed in both the brain and heart. 

An algorithm that integrates biomarkers for each of the proposed mechanisms for SUDEP will revolutionize our ability to predict and prevent SUDEP. Starting with the heart, we are testing whether alterations in cardiac and autonomic nervous system measures are associated with a high risk of SUDEP. Using the NIH funded Center for SUDEP Research database of multi-day recordings from multiple systems in ~1000 patients, we are investigating whether alterations in cardiac electrical and autonomic function serve as biomarkers associated with a high risk of future SUDEP.

Project 3: Novel Cardiac ECG-Based Methods to Distinguish Epileptic vs. Psychogenic Seizures

Seizures are classically thought to be due to electrical disturbances in the brain (epileptic seizures, ES), and recorded on the electroencephalogram (EEG). Yet, 30-40% of patients who are not controlled by anti-seizure medications do not have ES. The seizures have physical and behavioral manifestations indistinguishable from ES, but there are no EEG abnormalities. These non-epileptic seizure events are likely a response to emotional or social distress, and are called psychogenic non-epileptic seizures (PNES). The risks, treatments, and prognosis in ES vs. PNES differ substantially. Long-term inpatient video/EEG/ECG monitoring is the gold standard diagnostic test for discriminating between ES and PNES events. However, it is burdensome, expensive, often inconclusive, and not available in many affected populations worldwide. Thus, using in-house patient recordings and analytical tools, we are developing cost effective outpatient methods (wearable technology) and cardiac/autonomic measures to distinguish ES from PNES.


  1. Wang M, Szepietowska B, Polonsky B, McNitt S, Moss AJ, Zareba W, AUERBACH DS*. Risk of Cardiac Events Associated With Antidepressant Therapy in Patients With Long QT Syndrome. Am J Cardiol. 2018 Jan 15;121(2):182-187. PubMed PMID: 29174490; PubMed Central PMCID: PMC5742310.  *Corresponding author.
  2. AUERBACH DS*, Biton Y, Polonsky B, McNitt S, Gross RA, Dirksen RT, Moss AJ. Risk of cardiac events in Long QT syndrome patients when taking antiseizure medications. Transl Res. 2018 Jan;191:81-92.e7. PubMed PMID: 29121487; PubMed Central PMCID: PMC5733703.  *Corresponding author.
  3. Bao Y, Willis BC, Frasier CR, Lopez-Santiago LF, Lin X, Ramos-Mondragón R, AUERBACH DS, Chen C, Wang Z, Anumonwo J, Valdivia HH, Delmar M, Jalife J, Isom LL. Scn2b Deletion in Mice Results in Ventricular and Atrial Arrhythmias. Circ Arrhythm Electrophysiol. 2016 Dec;9(12)PubMed PMID: 27932425; PubMed Central PMCID: PMC5161227
  4. Carrell ST, Carrell EM,AUERBACH D, Pandey SK, Bennett CF, Dirksen RT, Thornton CA. Dmpk gene deletion or antisense knockdown does not compromise cardiac or skeletal muscle function in mice. Hum Mol Genet. 2016 Aug 13;PubMed PMID: 27522499. PubMed PMCID: PMC5291200
  5. AUERBACH DS*, McNitt S, Gross RA, Zareba W, Dirksen RT, Moss AJ. Genetic biomarkers for the risk of seizures in long QT syndrome. Neurology. 2016 Oct 18;87(16):1660-1668. PubMed PMID: 27466471; PubMed Central PMCID:PMC5085072. *Corresponding author.
  6. Stables CL, AUERBACH DS, Whitesall SE, D'Alecy LG, Feldman EL. Differential impact of type-1 and type-2 diabetes on control of heart rate in mice. Auton Neurosci. 2016 Jan;194:17-25. PubMed PMID:26725752; PubMed Central PMCID: PMC4724221
  7. Lin X, O'Malley H, Chen C, AUERBACH D, Foster M, Shekhar A, Zhang M, Coetzee W, Jalife J, Fishman GI, Isom L, Delmar M. Scn1b deletion leads to increased tetrodotoxin-sensitive sodium current, altered intracellular calcium homeostasis and arrhythmias in murine hearts. J Physiol. 2015 Mar 15;593(6):1389-407. PubMed PMID: 25772295; PubMed Central PMCID:PMC4376420
  8. AUERBACH DS, Jones J, Clawson BC, Offord J, Lenk GM, Ogiwara I, Yamakawa K, Meisler MH, Parent JM, Isom LL. Altered cardiac electrophysiology and SUDEP in a model of Dravet syndrome. PLoS One. 2013 Oct 14;8(10):e77843. PubMed PMID: 24155976; PubMed Central PMCID:PMC3796479
  9. Milstein ML, Musa H, Balbuena DP, Anumonwo JM, AUERBACH DS, Furspan PB, Hou L, Hu B, Schumacher SM, Vaidyanathan R, Martens JR, Jalife J. Dynamic reciprocity of sodium and potassium channel expression in a macromolecular complex controls cardiac excitability and arrhythmia. Proc Natl Acad Sci U S A. 2012 Jul 31;109(31):E2134-43. PubMed PMID: 22509027; PubMed Central PMCID:PMC3412015.
  10. Noujaim SF, Kaur K, Milstein M, Jones JM, Furspan P, Jiang D, AUERBACH DS, Herron T, Meisler MH, Jalife J. A null mutation of the neuronal sodium channel Nav1.6 disrupts action potential propagation and excitation-contraction coupling in the mouse heart. FASEB January 2012 26:63-72. PMID: 21948246; PubMed Central PMCID: PMC3250234
  11. AUERBACH DS, Jalife J. “Substrates and Triggers for the Initiation of Arrhythmias” Physiology News. Winter 2011. 85: 15–17
  12. AUERBACH DS, Grzeda KR, Furspan PB, Sato PY, Mironov S, Jalife J. Structural heterogeneity promotes triggered activity, reflection and arrhythmogenesis in cardiomyocyte monolayers. J Physiol. 2011 May 1;589(Pt 9):2363-81. PubMed PMID: 21486795; PubMed Central PMCID:PMC3098708
  13. Hou L, Deo M, Furspan P, Pandit SV, Mironov S, AUERBACH DS, Gong Q, Zhou Z, Berenfeld O, Jalife J. A major role for HERG in determining frequency of reentry in neonatal rat ventricular myocyte monolayer. Circ Res. 2010 Dec 10;107(12):1503-11. PubMed PMID: 20947828; PubMed Central PMCID:PMC3005848
  14. Noujaim SF, AUERBACH DS, Jalife J. Ventricular fibrillation: dynamics and ion channel determinants. Circ J. 2007;71 Suppl A:A1-11. PubMed PMID: 17587732
  15. Tanaka K, Zlochiver S, Vikstrom KL, Yamazaki M, Moreno J, Klos M, Zaitsev AV, Vaidyanathan R, AUERBACH DS, Landas S, Guiraudon G, Jalife J, Berenfeld O, Kalifa J. Spatial distribution of fibrosis governs fibrillation wave dynamics in the posterior left atrium during heart failure. Circ Res. 2007 Oct 12;101(8):839-47. PubMed PMID: 17704207
  16. Kalifa J, Tanaka K, Zaitsev AV, Warren M, Vaidyanathan R, AUERBACH D, Pandit S, Vikstrom KL, Ploutz-Snyder R, Talkachou A, Atienza F, Guiraudon G, Jalife J, Berenfeld O. “Mechanisms of Wave Fractionation at Boundaries of High Frequency Excitation in the Posterior Left Atrium of the Isolated Sheep Heart During Atrial Fibrillation” Circulation. Feb. 2006, 113(5): 626-633. PMID: 16461834
  17. Fonseca CA, AUERBACH DS, Suarez RV The Forensic Investigation of Propane Gas Asphyxiation. American Journal of Forensic Pathology. June 2002, 23(2) pp. 167–169. PMID: 12040262