Katharina Quinlan, PhD


Kathy Quinlan studies the neural basis of movement with a view to developing new biomarkers and pharmaceutical treatments for ALS, spinal muscular atrophy (SMA), and cerebral palsy. 

Her goal is to identify early morphological and electrophysiological changes that precede motor deficits. Since early changes in intrinsic properties appear while motor neurons are still functional, identification of early disease events could be useful for earlier clinical diagnosis. Targeting specific ion channels or synaptic pathways that set motor neurons on the course to dysfunction could lead to pharmaceutical approaches for treatment of these diseases.


The Quinlan lab’s focus is on the changes in the activity of spinal neurons in neurodegeneration and neural injury. Specifically, changes in intrinsic and synaptic drive to motoneurons are studied in cerebral palsy, ALS and spinal muscular atrophy. The ultimate goal is to translate findings from the lab to the clinic to improve biomarkers and improve therapies for these conditions.


Doctor of Philosophy, Marquette University, Milwaukee WI, 2004
Postdoctoral Fellow, Karolinska Institute, Stockholm, Sweden, 2004-2007
Research Associate, Northwestern University Feinberg School of Medicine, Chicago, IL 2007 – 2013
Research Assistant Professor, Northwestern University Feinberg School of Medicine, Chicago, IL 2013 – 2017

Selected Publications

Ziller, MJ, Ortega JA, Quinlan KA, Santos DP, Gu H, Martin EJ, Galonska C, Pop R, Maidl S, DiPardo A, Huang M, Meltzer HY, Gnirke A, Heckman CJ, Meissner A and Kiskinis E. Dissecting the functional consequences of de novo DNA methylation dynamics in human motor neuron differentiation and physiology. Cell Stem Cell 22: 1-16, 2018.

Quinlan KA, Kajtaz E, Ciolino JD, Manuel RD, Tresch MC, Heckman CJ and Tysseling VM. Chronic EMGs in treadmill running SOD1 mice reveal early changes in muscle activation. J Physiol 595:  5387-5400, 2017.

Drobyshevsky A and Quinlan KA. Spinal cord injury in hypertonic newborns after antenatal hypoxia-ischemia in rabbit cerebral palsy model. Exp Neurol 293:  13-26, 2017.

Quinlan KA, Lamano JB, Samuels J, and Heckman CJ. Comparison of dendritic calcium transients in juvenile wild type and SOD1G93A mouse lumbar motoneurons. Front Cell Neurosci 9: 139, 2015.

Drobyshevsky A, Takada S, Iuo K, Derrick M, Yu L, Quinlan KA, Vasquez-Vivar J, Nogueira MI, and Tan S. Elevated spinal monoamine neurotransmitters after antenatal hypoxia-ischemia in rabbit cerebral palsy model. J Neurochem 132:  394-402, 2015.

Shoenfeld L, Westenbroek RE, Fisher E, Quinlan KA, Tysseling VM, Powers RK, Heckman CJ and Binder MD. Soma size and Cav1.3 channel expression in vulnerable and resistant motoneuron populations of the SOD1G93A mouse model of ALS. Physiol Rep 2: 1-13, 2014.

Koschnitzky JE, Quinlan KA, Lukas TJ, Kajtaz E, Kocevar EJ, Mayers WF, Fu R, Siddique T, and Heckman CJ. Effect of fluoxetine on disease progression in a mouse model of ALS. J Neurophysiol 111: 2164-76, 2014.

Yasvoina M, Genc B, Jara J, Sheets P, Quinlan KA, Milosevic A, Shepherd GMG, Heckman CJ and Ozdinler PH. eGFP expression under UCHL1 promoter genetically labels corticospinal motor neurons and a subpopulation of degeneration resistant spinal motor neurons in an ALS mouse model. J Neurosci 33: 7890-904, 2013.

Tysseling VM, Janes L, Imhoff RD, Quinlan KA, Lookabaugh B, Ramlingam S, Heckman CJ, and Tresch MC. Design and evaluation of a chronic EMG multichannel detection system for long-term recordings of hindlimb muscles in behaving mice. J Electromyogr Kinesiol 23: 531-9, 2013.

Gogliotti RG, Quinlan KA, Barlow CB, Heier CR, Heckman CJ and DiDonato CJ. Motor neuron rescue in spinal muscular atrophy mice demonstrates that sensory-motor defects are a consequence, not a cause, of motor neuron dysfunction. J Neurosci 32: 3818-29, 2012.

Quinlan KA. Electrophysiological and molecular contributions to ALS pathology. Integr Comp Biol 51: 913-25, 2011.

Quinlan KA, Schuster JE, Fu R, Siddique T, and Heckman CJ. Altered postnatal maturation of electrical properties in spinal motoneurons in an ALS mouse model. J Physiol 589: 2245-60, 2011.

Heckman CJ, Mottram C, Quinlan K, Theiss R, and Schuster J. Motoneuron Excitability: The Importance of Neuromodulatory Inputs (Review). Clin Neurophyiol 120: 2040 – 54, 2009.

Crone SA*, Quinlan KA*, Zagoraiou L, Droho S, Restrepo CE, Lundfald L, Endo T, Setlak J, Jessell TM, Kiehn O, and Sharma K. Genetic Ablation of V2a Ipsilateral Interneurons Disrupts Left-Right Locomotor Coordination in Mammalian Spinal Cord. Neuron 60: 70-83, 2008.   (*equal authorship)

Stepien AE, Arber S. Probing the locomotor conundrum: Descending the ā€œVā€ interneuron ladder. Neuron 60: 1-4, 2008. Comment on above article

Quinlan KA* and Buchanan JT. Cellular and synaptic actions of acetylcholine in the lamprey spinal cord. J Neurophysiol 100: 1020-1031, 2008. *Corresponding author

Kiehn O, Quinlan KA, Restrepo CE, Lundfald L, Borgius L, Talpalar AE, and Endo T. Excitatory components of the mammalian locomotor CPG (Review). Brain Res Rev 57: 56-63, 2008.

Quinlan KA and Kiehn O. Segmental, Synaptic Actions of Commissural Interneurons in the Mouse Spinal Cord. J Neurosci 27: 6521- 6530, 2007.

Quinlan KA, Placas PG, and Buchanan JT. Cholinergic modulation of the locomotor network in the lamprey spinal cord. J Neurophysiol 92: 1536-1548, 2004.