About

Ayush Batra is an Associate Professor in the Department of Pathology and Neurology (Neurocritical Care) at Northwestern University Feinberg School of Medicine. He is affiliated with the Neurovascular Inflammation Lab and is involved in research within the Northwestern Medicine Doctor Profile Institutes and Centers, including the Center for Human Immunobiology, Northwestern University Clinical and Translational Sciences Institute (NUCATS), and the Robert J. Havey, MD Institute for Global Health (IGH). His work focuses on neurovascular inflammation, contributing to the understanding of inflammatory processes in neurological conditions. Batra's research aims to elucidate mechanisms underlying neurovascular inflammation, which may inform the development of therapeutic strategies for related diseases.

Research topics

• Internal medicine
• Medicine
• Pediatrics
• Sociology
• Virology
• Engineering
• Psychiatry
• Intensive care medicine
• Cardiology
• Emergency medicine
• Surgery
• Mathematics
• Demography

Selected publications

• Blood-Pressure Control after Intracerebral Hemorrhage — An Unbroken Glass Ceiling

  New England Journal of Medicine · 2026-04-22

  article1st authorCorresponding
  PublisherDOI

• Characterizing Neuro-PASC outcome with the mobile Neuro-COVID recovery care companion application

  BMC Neurology · 2026-01-12

  articleOpen access

  BACKGROUND: Long COVID, or post-acute sequelae of SARS-CoV-2 infection (PASC), affects 14 million people in the US. Neurologic manifestations of PASC (Neuro-PASC) are particularly debilitating. However, the evolution of these symptoms and factors associated with recovery are poorly understood. This study aimed to characterize Neuro-PASC symptom evolution using a mobile phone application and assess user experience. METHODS: The Neuro-COVID Recovery Care Companion (NCRCC) mobile application consists of questionnaires integrated within Northwestern Medicine's online MyChart platform which interfaces with the electronic medical record. Neuro-PASC patients completed daily surveys of twelve Neuro-PASC symptoms and their perceived percent recovery compared to their pre-COVID baseline. Patients also completed Patient-Reported Outcomes Measurement Information System (PROMIS) quality-of-life (QoL) surveys and NIH toolbox cognitive assessments at baseline and at 3-month follow up. Participants were retrospectively classified as "Improvers" or "Non-Improvers" based on the slope and range of their percent subjective recovery. RESULTS: Data from 63 participants presenting an average of 12.7 months after symptom onset were analyzed, including 27 (42.9%) Improvers and 36 (57.1%) Non-Improvers. Fewer women were Improvers (50% vs 75.7%; p = 0.04). Multiple correspondence analysis showed that patients presenting with a constellation of anosmia, dysgeusia, and a lack of insomnia (p = 0.023) were less likely Improvers. Improvers had more fluctuations in their subjective recovery than Non-Improvers with greater mean variance (7.01 vs 3.79; p = 0.0004) and positive recovery slope (5.84 vs 0; p < 0.0001). There were no differences in QoL and cognition at initial assessment, but Improvers showed a trend toward increased processing speed and decreased sleep disturbance after 3 months. Both groups found the NCRCC application easy-to-use, useful, and satisfactory. CONCLUSIONS: Our findings reveal previously unrecognized fluctuations in subjective recovery of Neuro-PASC, and that women and patients presenting with anosmia and dysgeusia are less likely to improve one year from COVID-19 onset. We found broad alterations in QoL in both groups suggesting that strategies to reduce sleep disturbance and improve cognition may contribute to subjective improvement. Our results suggest similar mobile applications may benefit patients with other ill-defined chronic diseases, by equipping and empowering them on their often windy road to recovery.

  PublisherOA PDFDOI

• Abstract A020: NR4A2-Driven Neutrophil Persistence in Aging Exacerbates Post-Stroke Inflammation and Injury

  Stroke · 2026-01-29

  articleSenior author

  Background: Neutrophils are the initial peripheral immune cells to be recruited following ischemic stroke, playing a dual role in tissue repair and injury. Elevated peripheral neutrophil counts correlate with larger infarct volumes and poorer outcomes, particularly in elderly patients. Aging alters neutrophil function, including increased expression of the nuclear transcription factor NR4A2, a regulator of cell survival and inflammation. We sought to investigate the role of NR4A2 in neutrophil recruitment, persistence, and function in aged brains following ischemic stroke using a murine transient middle cerebral artery occlusion (tMCAO) model. Methods: Young and aged Catchup (Ly6g-cre with a tdTomato reporter) mice were crossed with Nr4a2 floxed mice to generate Catchup Nr4a2-/- mice and were subjected to tMCAO for 90 minutes. Neutrophil infiltration and persistence were tracked through pulse labeling with 5-ethynyl-2’-deoxyuridine (EdU). Neutrophil distribution was quantified on coronal sections through wide-field immunofluorescence imaging at various timepoints. Results: Neutrophil distribution post-stroke was markedly altered in aged mice, with a higher concentration near the cortical surface at 72 hours (Fig. 1A and B), despite similar total counts. EdU labeling revealed that neutrophils infiltrated the brain within the first 24 hours and persisted for up to 120 hours post-stroke. EdU-positive cells replicated the spatial distribution of total neutrophils, confirming prolonged survival. Preliminary functional assays showed reduced metabolic activity in aged neutrophils, consistent with cellular senescence (Fig. 1C). Conclusion: Our findings demonstrate that aging alters neutrophil infiltration patterns and prolongs their survival in the infarcted brain, contributing to sustained inflammation and secondary injury. NR4A2 plays a critical role in regulating these processes, particularly in aged neutrophils. Future studies will explore the feasibility of targeting NR4A2 as a novel therapeutic target to mitigate age-related secondary injury.

  PublisherDOI

• Abstract A022: Spatiotemporal Dynamics of Monocyte-Derived Cells and Microglia in Post-Ischemic Stroke Inflammation and Recovery

  Stroke · 2026-01-29

  article

  Background: Ischemic stroke initiates a complex inflammatory cascade that contributes to both tissue repair and secondary injury, driven largely by resident microglia and monocyte-derived cells (MdCs). Microglia rapidly activate while recruited monocytes differentiate into diverse MdC subsets that can either promote recovery or exacerbate damage. The nuclear receptor NR4A1 (Nur77) has been identified as a key regulator of myeloid cell fate and function, but its role in post-stroke neuroinflammation remains unclear. Methods: To delineate the temporal dynamics of microglial and MdC responses following transient middle cerebral artery occlusion (tMCAO), we developed a novel dual-reporter mouse model and innovative tracking methods. This model uses adoptive bone marrow transfer and Cx3cr1- and Tmem119-cre drivers to discriminate between MdCs (Fig. 1A, green) and microglia (Fig. 1A, red) in real-time. Proliferating cells were pulse-labeled with 5-ethynyl-2’-deoxyuridine (EdU), which allows for longitudinal tracking of monocyte recruitment in addition to MdC and microglial expansion. EdU incorporation and NR4A1 protein expression were quantified with flow cytometry and population distributions were quantified using fluorescence microscopy. The effect of NR4A1 in microglia was interrogated using knockout (KO) recipients. Results: The analysis of EdU enrichment shows that MdCs are primarily derived from recently matured monocytes (Fig. 1B). Microglial proliferation was variable but correlated strongly with EdU+ MdC abundance, suggesting coordinated expansion. NR4A1 levels correlated strongly with the expansion of both MdCs and microglia. Deletion of Nr4a1 in microglia led to three times the MdC numbers compared to wild-type controls, supporting the role of NR4A1 in regulating MdC expansion (Fig. 1C). Taken together, these preliminary data suggest that NR4A1 deletion in microglia directly affects MdC recruitment and/or expansion. Conclusions: Our findings reveal a tightly regulated relationship between microglial and MdC expansion following ischemic stroke, with NR4A1 acting as a critical modulator of both cell types. NR4A1 appears to drive early MdC expansion while enhancing microglia expansion at later time points. Future studies will further investigate NR4A1’s cell-type-specific roles and explore its feasibility as a therapeutic target.

  PublisherDOI

• Toward development of a dynamic supramolecular peptide therapy for acute ischemic stroke

  Neurotherapeutics · 2026-01-01

  articleOpen accessSenior author

  <h2>Abstract</h2> Acute ischemic stroke (AIS) treatment relies on early restoration of blood flow; however, ischemia/reperfusion (I/R) may lead to secondary brain injury. Supramolecular peptide assemblies in which many molecules move collectively by design can activate key cellular pathways by displaying bioactive molecules on their surfaces. In this study, we hypothesized that a highly dynamic assembly formed by a peptide amphiphile (PA) that displays the laminin-mimetic sequence IKVAV (IKVAV-PA), known to promote neuron survival, could be delivered systemically, reach the ischemic brain, and exert therapeutic effects following AIS. C57BL/6 heterozygous CX3CR1^GFP mice underwent 60-min of transient middle cerebral artery occlusion and were administered IKVAV-PA or saline (control) immediately after reperfusion. IKVAV-PA presence and distribution was evaluated by intracranial intravital and wide-field imaging. Cresyl violet staining was performed to quantitate final brain infarct volume at 7 days post stroke. IKVAV-PA formed scaffolds that contain both nanoscale filaments in equilibrium with small micellar aggregates, which is a signature of enhanced epitope dynamicity. Systemically administered IKVAV-PA crossed the blood-brain barrier and was primarily detected within the ischemic hemisphere. Cresyl violet staining demonstrated IKVAV-PA treatment significantly reduced infarct size when compared to saline treated animals. Histological screening of systemic organs suggested good biocompatibility of IKVAV-PAs at 7 days post stroke. We demonstrated the therapeutic potential of systemically delivering IKVAV-PA in a pre-clinical model of ischemic stroke. This work lays the foundation for further studies utilizing supramolecular PA assemblies as an adjunct therapy to reperfusion therapies in order to enhance long-term tissue-level neural regeneration post stroke.

  PublisherOA PDFDOI

• Standard complete blood count to predict long‐term outcomes in febrile infection–related epilepsy syndrome (FIRES): A multicenter study

  Epilepsia · 2025-08-22 · 3 citations

  articleOpen access

  OBJECTIVE: We investigated whether complete blood count (CBC) analyses during intensive care unit stay could predict 12-month outcomes in patients with cryptogenic febrile infection-related epilepsy syndrome (FIRES), a subset of new-onset refractory status epilepticus (NORSE). METHODS: Outcomes at 12 months were classified as "unfavorable" (Glasgow Outcome Score [GOS] 1-3) or "favorable" (GOS 4-5). Demographic, clinical, and serial CBC data were collected across treatment phases: (1) no immunotherapy (before initiation or no treatment), (2) first-line immunotherapy, and (3) second-line immunotherapy. For each treatment phase, predictive models stratified outcomes based on CBC features using decision tree regression, with separate models for adults and children. Model performance was tested using a leave-one-patient-out approach. RESULTS: We studied 63 patients (34 adults, 29 children) from 12 centers. Unfavorable outcomes occurred in 18 adults and 12 children. Children were more likely to receive second-line immunotherapy. We analyzed 1530 CBCs (adults: 997 CBCs, including 539 for unfavorable outcomes; children: 533 CBCs, including 415 for unfavorable outcomes). Subgroup analyses revealed differences in CBC levels according to the outcomes and the treatment received. Adults with unfavorable outcomes notably had higher neutrophil-to-lymphocyte ratios (NLRs) and monocyte-to-lymphocyte ratios (MLRs), whereas children with unfavorable outcomes had higher red cell distribution width. NLRs and MLRs increased when CBCs were collected after the initiation of immunotherapy for both adults and children. The variables of interest differed in the different predictive models but always included the proportion of at least one subtype of leukocyte. Prediction accuracy with our models was higher in children (87% overall, with the best performance in no-treatment and first-line phases) than in adults (83% overall, with the best performance during/after the initiation of second-line). SIGNIFICANCE: Findings suggest the potential for standard CBCs to serve as a rapid, accessible tool for early prognostication in cryptogenic FIRES, particularly in children.

  PublisherOA PDFDOI

• Injury to repair: Functions of microglia and monocyte-derived cells in ischemic stroke

  Journal of Stroke and Cerebrovascular Diseases · 2025-09-17

  articleOpen accessSenior author

  INTRODUCTION: Microglia, the central nervous system's resident immune cells, play a complex role in acute ischemic stroke (AIS), contributing to both neuroprotection and secondary neurologic injury. After ischemic injury, microglia activate and adopt a diverse range of phenotypes, from extremes of pro-inflammatory to anti-inflammatory microglia. Coinciding with microglial activation, AIS triggers infiltration of monocytes, which transform into monocyte-derived cells (MdCs) within the ischemic microenvironment. MdCs display many overlapping characteristics with microglia, complicating their identification and role in recovery. METHODS: This narrative review synthesizes current basic and translational research examining the heterogeneity and interplay of microglia and MdCs in response to AIS. Relevant literature was identified through a comprehensive search of the PubMed database, inclusive of studies published through June 2025. RESULTS AND CONCLUSIONS: Anti-inflammatory microglial phenotypes promote neuronal survival, phagocytosis of necrotic debris, and blood-brain barrier repair. Pro-inflammatory microglial phenotypes, conversely, exacerbate injury through excitotoxicity, cytokine release, and vascular disruption. Initially, MdCs adopt a neuroprotective, reparative microglia-like role by phagocytizing debris and supporting repair but later shift to a pro-inflammatory phenotype, driving secondary damage. The dynamic interaction between microglia and MdCs is crucial for stroke recovery, with microglia and MdCs initially aiding in tissue repair and angiogenesis while subsequently amplifying secondary injury through pro-inflammatory phenotypes. Although various biomarkers have been proposed to differentiate microglia from MdCs and predict stroke outcomes, none have been clinically validated. Further studies are needed to identify reliable biomarkers for these distinct cell types and develop strategies to minimize secondary injury without impairing recovery after stroke.

  PublisherOA PDFDOI

• Abstract WP371: Cranial bone marrow-derived polymorphonuclear neutrophils comprise a small fraction of infiltrating leukocytes within the ischemic cortex following ischemia/reperfusion injury.

  Stroke · 2025-01-30

  article1st authorCorresponding

  Introduction: The cranial bone marrow has been recognized as a potential reservoir for myeloid cells, capable of entering the cerebral cortex through direct channels connecting the skull and cortical surface of the brain. The significance of cranial bone marrow-derived leukocytes following ischemic stroke in the setting of ischemia/reperfusion remains uncertain. We sought to characterize the fraction of cranial bone marrow-derived leukocytes entering the ischemic cortex following ischemia/reperfusion injury using a murine transient middle cerebral artery occlusion (tMCAO) model. Methods: C57BL/6 LysM-GFP (green neutrophils and monocytes) mice underwent gamma irradiation with and without head shielding prior to adoptive transfer of bone marrow harvested from heterozygous CatchUp mice (Ly6G-tdTomato, red neutrophils). As a result, the exact percentages of cranial- and peripheral-derived neutrophils could easily be quantified and tracked, both in circulation and in the post-mortem brain. Mice underwent 90 min tMCAO with peripheral blood collection prior to and at 24 hours following ischemia/reperfusion. The relative fractions of green and red fluorescent Lys6G+ neutrophils post tMCAO in the brain were compared to the blood using flow cytometry and wide field fluorescence microscopy. Results: The ratio of red and green Ly6G+ neutrophils in the brain most closely matched the ratio of circulating red and green neutrophils and was not particularly enriched in GFP+ neutrophils. The distribution of red and green cells in brain tissue was nearly identical and did not show an enrichment of either blood-derived or cranial bone marrow-derived cells in any particular region following tMCAO at 24 hours. Conclusions: Together these data suggest that the majority of neutrophils entering the brain at 24 hours following stroke come from circulation with only a small contribution of neutrophils arriving directly from the cranial bone marrow. Furthermore, the distribution of red and green cells in tissue suggests that the neutrophils intermix regardless of origin. Further studies evaluating the subset of cranial bone marrow-derived neutrophils are needed to understand their significance specific to ischemia/reperfusion injury.

  PublisherDOI

• EdU tracking of leukocyte recruitment in mouse models of ischemic stroke and sterile lung inflammation

  Journal of Cell Science · 2025-04-15 · 6 citations

  articleOpen access

  The discovery of copper(I)-catalyzed azide-alkyne cycloaddition (click chemistry) has significantly advanced the detection of proliferating cells by utilizing 5-ethynyl-2'-deoxyuridine (EdU). EdU, a thymidine analogue, is incorporated into DNA during replication and detected by the direct reaction with an azide-conjugated fluorophore. Traditionally, dividing cells are labeled using 5-bromodeoxyuridine (BrdU), another nucleotide analogue. However, BrdU detection is a harsh method that requires substantial sample processing, unlike EdU detection. EdU is classically used to identify proliferating cells; however, we report a streamlined methodology that uses EdU to label and track leukocyte recruitment that is compatible with flow cytometry and microscopy and preserves transgenic fluorophores. EdU labeling was performed in two different models of sterile inflammation: ischemic stroke and hydrochloric acid aspiration. EdU injection was timed to differentially label circulating monocytes, neutrophils and T cells. Tissue analysis showed EdU-positive monocytes and T cells were enriched in both inflammatory models. This suggests that recently divided monocytes and T cells are preferentially recruited to these vascular beds during inflammation and highlights the utility of this labeling approach to track leukocyte subtypes longitudinally during inflammation.

  PublisherOA PDFDOI

• 758: ATYPICAL ETIOLOGY OF LIDOCAINE TOXICITY PRESENTING AS BRADYCARDIA AND STATUS EPILEPTICUS

  Critical Care Medicine · 2025-01-01 · 1 citations

  articleSenior author
  PublisherDOI

Frequent coauthors

• Eric M. Liotta

  37 shared

• René A. Colorado

  Arcadia

  25 shared

• Anna M. Bank

  Lenox Hill Hospital

  25 shared

• Jeffrey R. Clark

  Columbia University Irving Medical Center

  23 shared

• Igor J. Koralnik

  Northwestern University

  22 shared

• Joseph F. Rizzo

  16 shared

• Alice Lam

  Massachusetts General Hospital

  16 shared

• Emer R. McGrath

  Framingham Heart Study

  16 shared