Gabriela I. Aparicio, Ph.D. is a Postdoctoral Scholar in the Department of Neurosurgery at the University of Kentucky. She earned her Ph.D. in Molecular Biology and Biotechnology from the National University of San Martín in Argentina and specializes in cellular and molecular neuroscience. Her research focuses on Schwann cell biology, nerve regeneration, and the development of in vitro models for studying peripheral nerve degeneration. Gabriela has extensive expertise in molecular biology, histology, fluorescence microscopy, and spatial transcriptomics. She has published in leading journals and presented at international conferences, contributing to advancements in regenerative medicine and neuroplasticity.

Peripheral nerves display a remarkable ability for self-repair. Studies in experimental animals have delineated our understanding of the mechanisms governing nerve degeneration and regeneration in the mammalian peripheral nervous system (PNS) but human data is still incomplete. The lack of technologies to perform cellular and molecular studies in human nerves, along with ethical and practical challenges, have limited our collective advancement of basic and translational human PNS research. Schwann cells have attracted much attention over the years at least in part because of their plasticity to convert into repair cells and drive axonal regrowth. Yet, adult human nerves contain assorted supporting cell populations exhibiting strong pro-regenerative transcriptional and immunological signatures which have been understudied in comparison to Schwann cells. This project aims to study the phenotype and function of human nerve cells and their responses to injury by using an organotypic model of human tissue culture that recapitulates key events of Wallerian degeneration in a dish. We will investigate the time course of axonal degeneration in motor and sensory nerves and how this relates to myelin clearance, cell reprogramming, and extracellular matrix remodeling mediated by endogenous Schwann cells and other nerve-resident cells from the endo-, peri-, and epineurium. We hope this project advances our understanding of nerve regeneration in humans while contributing to the design of better treatment options for traumatic nerve injuries and degenerative diseases.

Jason Chua, M.D., Ph.D., is an Assistant Professor of Neurology in the Johns Hopkins School of Medicine. Prior to joining the faculty at Johns Hopkins, Dr. Chua completed his MD, PhD, neurology residency, and movement disorders fellowship at the University of Michigan. Currently, he is a physician-scientist serving as both a neurologist in the Johns Hopkins Parkinson's Disease and Movement Disorders Center, and as a Principal Investigator in the Johns Hopkins Institute for Cell Engineering. Dr. Chua's laboratory focuses on the roles of autophagy in neurodegenerative diseases, using induced pluripotent stem cell-derived neurons to model neurological disorders and discover novel and neuron-specific mechanisms that are targetable for therapy design.

Paclitaxel (PTX) is a widely used chemotherapy drug, but it often causes paclitaxel-induced peripheral neuropathy (PIPN)—a painful condition that can limit cancer treatment. Currently, there are no FDA-approved therapies to prevent or treat PIPN, and the underlying molecular mechanisms remain unclear.

Our research focuses on how PTX triggers nerve damage. While PTX stabilizes microtubules in cancer cells, its neurotoxic effects involve additional signaling pathways, including a Wallerian-like axonal degeneration cascade. Preliminary findings show that MAP4K proteins play a key role in this process, and blocking them can protect neurons in both lab and animal models. However, the upstream triggers that activate MAP4Ks are unknown.

We hypothesize that PTX interacts with specific neuronal proteins that activate MAP4K signaling, leading to axonal degeneration. Using phospho-proteomics, siRNA knockdown, and a novel affinity chromatography approach, we aim to identify these proteins. Our ultimate goal is to discover new drug targets to prevent nerve damage and improve cancer care.

Aysel Fisgin, Ph.D., received her BS degree in Chemical Engineering at Middle East Technical University, Turkey, in 1993. After 15 years of working as a professional in industry, then starting up and managing her own business, she started graduate school and got her MS degree in Medical Systems and Informatics from Bogazici University, Turkey. She pursued her Ph.D. in Biomedical Engineering at Bogazici University in Turkey till she moved to the US in 2013. She received a European Union Marie Curie Actions IRSES Project scholarship and carried out her Ph.D. thesis experiments in Biomedical Engineering, Johns Hopkins University. Her Ph.D. thesis research is on high throughput drug screening against CIPN (Chemotherapy-Induced Peripheral Neuropathies).

She completed her post-doctoral research fellowship in Hoke Lab, Neurology, Johns Hopkins University and currently works as a research associate in Hoke Lab. She works on in-vitro and invivo peripheral neuropathy models of different chemotherapy drugs and transgenic mice that are resistant to the development of neuropathies caused by these chemotherapy agents. Her research focus is on understanding mechanisms of peripheral neuropathies and identifying therapeutic drugs that can be co- or pre-administered to cancer patients with chemotherapy agents before axonal degeneration starts.

Paclitaxel (PTX) is a widely used chemotherapy drug, but it often causes paclitaxel-induced peripheral neuropathy (PIPN)—a painful condition that can limit cancer treatment. Currently, there are no FDA-approved therapies to prevent or treat PIPN, and the underlying molecular mechanisms remain unclear.

Our research focuses on how PTX triggers nerve damage. While PTX stabilizes microtubules in cancer cells, its neurotoxic effects involve additional signaling pathways, including a Wallerian-like axonal degeneration cascade. Preliminary findings show that MAP4K proteins play a key role in this process, and blocking them can protect neurons in both lab and animal models.

However, the upstream triggers that activate MAP4Ks are unknown. We hypothesize that PTX interacts with specific neuronal proteins that activate MAP4K signaling, leading to axonal degeneration. Using phospho-proteomics, siRNA knockdown, and a novel affinity chromatography approach, we aim to identify these proteins. Our ultimate goal is to discover new drug targets to prevent nerve damage and improve cancer care.

Timothy J. Hines, Ph.D. is a Postdoctoral Associate with Dr. Robert Burgess at The Jackson Laboratory for Mammalian Genetics in Bar Harbor, ME. Tim completed his doctoral training in 2018 with Dr. Deanna Smith at the University of South Carolina where he studied the regulation of microtubule-based axonal transport by posttranslational modifications and protein-protein interactions. Since starting his postdoc, he has characterized numerous mouse models of neuromuscular diseases including multiple forms of Charcot-Marie-Tooth disease (CMT), spinal muscular atrophy with respiratory distress (SMARD), congenital myopathy, and ataxia.

Tim’s current research investigates the role of the integrated stress response (ISR) in inherited neurodegenerative diseases, with a focus on the transcription factor, ATF4. In 2023, he received a K99/R00 through the NIH’s Maximizing Opportunities for Scientific and Academic Independent Careers (MOSAIC) program to support his research combining mouse models and human iPSC-derived motor neurons to explore how ATF4 and downstream changes in gene expression are regulated in forms of CMT caused by mutations in tRNA synthetase genes. His recent results demonstrate that ATF4 expression is both necessary and sufficient to drive CMT-like phenotypes in mice. Through this work, Tim aims to identify novel therapeutic targets that could potentially benefit patients across a range of neurodegenerative diseases characterized by ISR activation.

This project has two primary goals. The first is to determine if the aaRS-CMT mechanisms that have been identified in mouse models (i.e. ISR activation and ATF4 expression) are relevant in human motor neurons with aaRS-CMT mutations. The second is to elucidate the regulatory dynamics of the transcription factor ATF4, whose expression is both necessary and sufficient to induce CMT phenotypes in mice. Whether the transcriptional program induced by ATF4 is regenerative or leads to apoptosis is influenced by ATF4 localization, posttranslational modifications (PTMs), protein-protein interactions (ATF4 heterodimerizes to alter gene expression), and chromatin accessibility/DNA binding.

To accomplish these goals, we will use human iPSC-derived motor neurons with aaRS-CMT mutations and a HaloTagged ATF4 knocked into the endogenous ATF4 locus. The HaloTag will allow us to interrogate each of these points through live-cell imaging (ATF4 expression and localization), immunoprecipitations (for PTMs and dimerization partners), and CUT&RUN-sequencing (for chromatin accessibility and DNA binding). These studies will provide mechanistic insight into ATF4-mediated neurodegeneration and identify candidate therapeutic targets for future intervention.

Maaz Khan, M.D., M.A. (Cantab), M.R.C.S. (RCSEng), grew up in Leicester, England. He completed his undergraduate and medical degrees in the six-year accelerated medicine program at the University of Cambridge, UK. He graduated as the top-ranking student in his BA and received numerous awards throughout his six years at the University of Cambridge, including the prestigious Passingham Prize, the Ronald Greaves Award and the Clinical School Leadership Prize.

Remarkably, at the age of 21, while still a medical student, he was invited to teach neuroscience to undergraduate students at the University of Cambridge, becoming one of the youngest teachers in the history of the university.

After graduating from medical school, Dr. Khan worked as a physician at the University of Oxford John Radcliffe Hospital and was subsequently appointed as a clinical examiner. He also delivered tutorials and seminars to the medical students at the University of Oxford.

Since starting medical school, Dr. Khan has conducted neurosurgical research at various prestigious institutions, including the University of Cambridge, Harvard Medical School and Boston Children's Hospital. He is now working as a post-doctoral research fellow at Johns Hopkins University and focuses on traumatic peripheral nerve injury.

Additionally, he was appointed as a guest lecturer in the undergraduate and master's neurosciences program at Johns Hopkins University and has been invited as a session chair and speaker at numerous international conferences. Most notably, at the Peripheral Nerve Society 2025 Annual Meeting he was awarded the Jack Griffin Prize for delivering the best oral presentation on traumatic and toxic neuropathy.

Peripheral nerve injuries affect over 20 million people in the U.S., causing chronic pain, loss of movement, and lifelong disability. These injuries significantly reduce quality of life and contribute to annual healthcare costs exceeding $150 billion. While peripheral nerves have some capacity for regeneration after acute injury, this ability declines with prolonged denervation, especially in severe or proximal injuries.

Our world-renowned peripheral nerve surgery team performs approximately 100 cases per year and has built a unique biobank of human nerve and muscle tissue samples from patients undergoing surgery. This project leverages these samples to investigate how human nerve and muscle tissues change at the molecular level following injury.

Using single-nucleus RNA sequencing (snRNA-seq) and bulk RNA sequencing (bulkRNA-seq), we aim to:

• Identify gene expression changes in specific cell subtypes over time.
• Understand the cellular and molecular mechanisms driving degeneration and regeneration.
• Discover novel therapeutic targets to enhance recovery after nerve injury.

Dr. Raniki Kumari is a postdoctoral fellow in the Department of Biology at Johns Hopkins University. She earned her PhD from the Regional Center for Biotechnology in Faridabad, India. During her doctoral studies, she studied a previously uncharacterized amyloidogenic protein known as OTU de-ubiquitinase ubiquitin aldehyde binding 1 (OTUB1). Her research revealed that OTUB1, which functions as a de-ubiquitinase, has the propensity to form amyloid aggregates in mammalian cell cultures, as well as in a mouse model of Parkinson’s disease, leading to neurotoxicity. This work was published in the Journal of Biological Chemistry in 2020. Dr. Kumari further demonstrated that OTUB1 undergoes S-nitrosylation under redox stress conditions, enhancing its aggregation and contributing to neuronal toxicity, a finding published in ACS Chemical Neuroscience in 2022.

In 2021, Dr. Kumari joined the laboratory of Dr. Rejji Kuruvilla at Johns Hopkins University as a postdoctoral fellow. Her research focuses on the development and functions of the sympathetic nervous system. In a recent publication in Cell Reports (2024), she demonstrated that sympathetic neurons expressing the neuropeptide, Neuropeptide Y (NPY), innervate blood vessels in peripheral organs and regulate metabolic and cardiovascular functions in mice. In her latest work (in press, Cell Reports), she identified a contact-mediated pathway governing sympathetic neuron and satellite glial cell interactions, which are crucial for neuronal morphology, neurotransmitter homeostasis, neuronal activity, and autonomic functions in mice.

Currently, Dr. Kumari is investigating the resilience of sympathetic neurons compared to sensory neurons when exposed to circulating neurotoxins, such as the chemotherapeutic agent Bortezomib (BTZ). While BTZ causes significant damage to sensory neurons, preliminary results suggest that sympathetic neurons are relatively protected, likely due to non-neuronal cells (satellite glial cells) that form a barrier shielding them from systemic insults. Using genetic mouse models, advanced imaging, transcriptomics, and cellular assays, Dr. Kumari is dissecting the molecular and cellular mechanisms by which satellite glial cells provide this protection.

This project investigates the molecular mechanisms underlying the selective vulnerability of sensory neurons to Bortezomib (BTZ), a commonly used chemotherapeutic agent in hematological cancers, which frequently causes peripheral neuropathy in up to 80% of patients. While sensory neurons, particularly in the somatosensory system, are predominantly affected by BTZ, sympathetic neurons appear to be relatively spared.

The goal of this project is to characterize the cellular and molecular pathways that contribute to the enhanced susceptibility of sensory neurons to BTZ relative to sympathetic neurons. The project will use genetic mouse models, advanced imaging, transcriptomics, and cellular assays.

The significance of this research lies in its potential to improve treatment strategies for chemotherapy-induced peripheral neuropathy and provide fundamental insights into the broader mechanisms of neuronal susceptibility in neurodegenerative disorders. Understanding these molecular processes may lead to novel therapeutic targets that can mitigate the damaging effects of chemotherapy on specific neuronal populations.

Jing Liu, M.D., M.S., Ph.D., is a postdoctoral research fellow in the Department of Anesthesiology and Critical Care Medicine at Johns Hopkins University School of Medicine. With prior clinical experience as an attending neurologist and doctoral training in neurobiology, her research focuses on how immune cells and sensory neurons interact in neuropathic disorders, including chemotherapy-induced peripheral neuropathy (CIPN) and inflammation-related sensory dysfunction. She studies how peripheral immune signals influence dorsal root ganglion (DRG) neuron activity and contribute to pathological sensory processing.

Jing uses in vivo and in vitro calcium imaging, molecular and cellular assays, and quantitative behavioral approaches to identify the receptors and pathways involved in neuroimmune communication, including the mast-cell specific MrgprB2 and MrgprX2 receptors. By defining how different chemotherapeutic agents engage these mechanisms, her work aims to clarify why certain treatments lead to persistent sensory disturbances and to identify opportunities for non-opioid therapeutic intervention.

Her long-term goal is to establish an independent research program focused on cell-type specific mechanisms underlying neuropathic disorders and on translating mechanistic insights into targeted treatments that improve clinical outcomes for patients affected by sensory system disease.

Chemotherapy-induced peripheral neuropathy (CIPN) is a debilitating and common treatment-limiting side effect, yet effective non-opioid therapies remain lacking. Mast cells (MCs) are resident immune cells that modulate neuroimmune signaling and contribute to CIPN, but the specific receptors and pathways driving their activation remain unclear. Mas-related G-protein-coupled receptor B2 (MrgprB2) and its human orthologue MrgprX2 are newly identified MC-specific receptors that trigger robust degranulation in response to basic secretagogues.

This project will define the roles of MrgprB2 and MrgprX2 in CIPN pain across multiple chemotherapies using mouse genetic models, humanized MrgprX2 mice, and selective antagonists. We aim to map MC activation in vivo, identify when MrgprB2/X2 signaling is required, and determine the optimal timing and strategy for receptor blockade to prevent oxaliplatin-induced neuropathic pain.

By establishing how specific chemotherapeutic agents engage MrgprB2/X2 pathways, this work seeks to create a mechanistic and precision-guided foundation for developing targeted, non-opioid CIPN pain therapies.

Dr. Mehmet Can Sari earned his medical degree with honors from Hacettepe University School of Medicine in Turkey in 2023. He is currently a postdoctoral research fellow in the Hoke Lab at the Johns Hopkins University School of Medicine, Department of Neurology, where his work focuses on peripheral nerve regeneration.

Dr. Sari’s research centers on the developmental and regenerative roles of mRNA methylation in Schwann cells, particularly the m6A “writer” enzyme METTL14. Using conditional knockout mouse models and advanced transcriptomic approaches, he investigates how epitranscriptomic regulation shapes Schwann cell injury responses and nerve repair.

He has authored peer-reviewed research articles, reviews and his work has been recognized with multiple awards, including Abstract of Distinction and Travel Awards from the American Neurological Association and support from the Merkin Microgrant Program. Dr. Sari aims to become a physician-scientist neurologist specializing in peripheral nerve disorders, bridging mechanistic discovery with translational therapies for patients with neuropathy and nerve injuries.

Peripheral nerve injuries and neuropathies affect millions of people and often lead to chronic disability, yet current treatments do not directly enhance the nerve’s intrinsic ability to repair itself. This project focuses on a chemical modification on mRNA called N6-methyladenosine (m6A), which acts as a rapid regulatory “switch” that controls RNA stability and translation.

Preliminary work from Dr. Sari and colleagues shows that m6A levels in Schwann cells-glial cells that support and myelinate peripheral nerves-increase rapidly after sciatic nerve injury. Loss of the m6A “writer” enzyme METTL14 in Schwann cells leads to progressive demyelination, impaired regeneration, and blunted induction of key repair genes, suggesting that m6A is essential for an effective injury response.

Using sciatic nerve injury models across the lifespan and long read RNA sequencing, this project will map m6A changes after injury and integrate them with gene expression profiles to identify core regenerative pathways. Another focus is on how m6A regulates Glial cell line-derived neurotrophic factor (GDNF), a potent pro-regenerative factor that supports axonal survival and regrowth.

By defining how m6A controls Schwann cell repair programs, this work aims to establish a foundation for RNA-targeted therapies to improve nerve regeneration and outcomes for patients with peripheral nerve injuries and neuropathies.

Dr. Sana Sarkar is a neuroscientist whose research focuses on peripheral nerve regeneration and neuropathies, including diabetic and chemotherapy-induced neuropathy. Her work investigates the role of lactate-specific monocarboxylate transporters (MCTs) in cellular metabolism and nerve repair, using transgenic mouse models and primary cultures. Dr. Sarkar earned her Ph.D. in Biotechnology from Integral University, India, where she explored mitochondrial dynamics, cellular bioenergetics, and epigenetic regulation in neurodegeneration. She has published extensively on microRNA-mediated regulation in neurotoxicity and neurodegenerative diseases and co-authored a patent for an innovative biomolecule staining system. Her research aims to identify novel therapeutic strategies that bridge basic neuroscience with clinical applications.

Current therapies for peripheral nerve injury struggle due to slow axonal regrowth (~1 mm per day), prompting increased focus on understanding nerve repair mechanisms and developing effective strategies. MicroRNAs (miRNAs), which display distinct temporal expression patterns across the key phases of peripheral nerve regeneration, represent a promising yet underexplored avenue. Our preliminary studies have shown that Schwann cell (SC)-specific monocarboxylate transporters (MCT 1, 2, and 4) are essential for effective nerve regeneration. Ablation of these transporters in mice impairs regeneration and reduces c-Jun expression in SCs, indicating a compromised switch to the repair phenotype. Studies indicate that c-Jun is crucial for post-transcriptional regulation of repair programs, controlling over 100 genes and miRNAs in repair SCs. We have collected single-nucleus RNA-sequencing (snRNA-seq) data from uncrushed sciatic nerves, as well as nerves at 3 and 7 days after crush injury, in both wild-type and P0:MCT TripleFlox mice.

The current project aims to profile miRNA expression in sciatic nerves of wild-type and P0:MCT TripleFlox mice in uninjured and 3- and 7-day post-crush conditions. Further, miRNA expression profiles will be integrated with snRNA-seq data to identify miRNA-mRNA regulatory modules. The roles of top candidates will also be exclusively examined through gain and loss-of-function approaches, both in vitro and in vivo. This integrative approach will reveal key regulatory nodes for improving regenerative outcomes in peripheral nerve injury.

Ligia obtained her dental and master’s degrees at the University of São Paulo, Brazil. She conducted her PhD in the Oral Health Sciences Program at the University of Michigan School of Dentistry. Her PhD work focused on cancer neuroscience and the investigation of nerve-tumor interactions, specifically in the context of oral cavity cancer. As a postdoctoral fellow in Roman Giger’s lab, her research focuses on understanding the molecular mechanisms that control Schwann cell plasticity during nerve repair, with a particular emphasis on how these cells interact with axons and the immune system to influence regeneration and pain.

Injuries to peripheral nerves are common and can lead to lifelong problems, such as difficulty moving or feeling, or even chronic pain. In my early research, I found that Schwann cells, which help protect and repair nerves, quickly begin producing a protein called sonic hedgehog (Shh) after an injury, even before nerves start to break down. By studying nerve tissue at the single-cell level and using special reporter mice, I discovered that another group of cells in the nerve, called endoneurial mesenchymal cells (eMES), are the main cells that respond to Schwann cell signals. My results also support that eMES may be responsible for attracting immune cells to the injury and controlling inflammation in the nerve, but the consequences for regeneration are unknown. To understand the role of Shh-activated eMES in functional recovery after injury, I will analyze which immune cells infiltrate the nerve, evaluate nerve regeneration, and assess pain in the absence of Shh. This research will help better understand how Schwann cells and eMES interact after a nerve injury, potentially opening new ways to treat nerve damage and pain. Instead of focusing only on Schwann cells, this work emphasizes the importance of how different cell types interact in healing and inflammation after nerve injury.

Dr. Lauren S. Vaughn is currently a Research Assistant Professor in the Department of Biological Sciences at the University of South Carolina. She holds a BSc in Biology from the University of Texas at Dallas and a PhD in Biological Sciences from the University of South Carolina where she was awarded their prestigious Presidential Fellowship. Her graduate work under Dr. Rekha C. Patel focused on changes in stress signaling due to mutations found in DYT16 dystonia. She then performed her post-doctoral work at Columbia University where she was awarded an NIH Ruth L. Kirchstein National Research Service Award (NRSA) Institutional Research Training Grant (T32) to study molecular signaling of macrophages during sepsis. Currently, she works under Dr. Jeff Twiss studying the varying mechanisms controlling local translation after mechanical injury stress in peripheral axons.

The objectives of this study are to identify the contribution of local translation in the development of chemotherapy-induced peripheral neuropathy (CIPN). Insults like crush injury or chemotherapy agents can place additional stress on neurons that bring the need for rapid and specific local synthesis of new proteins as axonally synthesized proteins support growth, survival, and function of axons. Regulation of local translation is dictated by mRNA localization, storage, and translation efficiency. Stress granules (SG) play a key role in regulating protein synthesis in axons by storing mRNAs during periods of cell stress. It is not known how different chemotherapeutic agents affect stress pathways and axonal translation in adult neurons, though decreased mRNA transport has been linked to CIPN. Insight into the development and progression of the axonal pathology in CIPN will inform potential future therapeutics to prevent axon degeneration.

• Maaz Khan, M.D. | Topics:
  • Single nuclear RNA sequencing in the rat gastrocnemius muscle following acute and chronic peripheral nerve injury and the temporal correspondence of the gene expression profile with human denervation
  • Single nuclear RNA sequencing in the rat sciatic nerve following acute and chronic peripheral nerve injury and the temporal correspondence of the gene expression profile with human denervation
  • Evaluating the pathophysiology of aging and senescence using single nuclear RNA sequencing in mouse distal sciatic nerve and gastrocnemius muscles following acute and chronic peripheral nerve injury
• Arens Taga, M.D.
  • Topic: Investigating the role of β1-importin in axonal regeneration of human spinal motor neurons, using an in vitro microfluidic and human induced pluripotent stem cell (hiPSC)-based platform
• Athanasios Alexandris, M.D.
  • Topic: Investigating a Novel Regulator of SARM1-Dependent Neurodegeneration
• Bipasha Mukherjee-Clavin, M.D., Ph.D.
  • Topic: Exploring early molecular abnormalities in CMT1A
• Diana Tavares Ferreira, Pharm.D., Ph.D.
  • Topic: RNA transport as a key to axonal integrity in peripheral neuropathies
• Patricia Jillian Ward, Ph.D.
  • Topic: Mechanisms and consequences of post-ganglionic sympathetic axon regeneration following injury 
• Jorge Gomez Deza, Ph.D.
  • Topic: Identifying novel therapeutic targets for CIPN using iPSC-derived neurons
• Masnsen Cherief, Ph.D.
  • Topic: Advanced In Silico Analysis and Therapeutic Approaches for Diabetic Peripheral Neuropathy and Bone Disease

• Ayobami Ward, M.D., Sc.M.
  Topic: Age-Dependent Nerve Regeneration Mechanisms: Focus of the Human Repair Schwann Cell Phenotype
• Aysel Fisgin, Ph.D.
  Topic: Inhibition of TNIK is a promising therapeutic approach for PIPN
• Jeremy Sullivan, Ph.D.
  Topic: Molecular mechanisms of TRPV4-mediated motor axon degeneration
• Jesse Stokum, M.D., Ph.D.
  Topic: Enhanced Peripheral Neural Regeneration with Limb Lengthening
• Kathryn Moss, Ph.D.
  Topic: Exploring Functional Demyelination Pathomechanisms for CMT1A and HNPP Caused by Node of Ranvier Defects
• Sachin Gadani, M.D., Ph.D.
  Topic: Exploring the role of alarmins on immune recruitment after peripheral nerve injury
• Wonjin Yun, Ph.D.
  Topic: Modeling CMT1A with a novel macrophage-integrated neural crest organoids (MINOs) and interrogating cell therapy efficacy of hypoimmunogenic induced human Schwann cells.
• Xuewei Wang, Ph.D.
  Topic: Elucidating the mechanisms by which H3K27me3 maintains normal axon regeneration.
• Yu Su, M.D., Ph.D.
  Topic: Targeting Glutamate Carboxypeptidase II (GCPII) to Enhance Nerve Remyelination and Recovery Following Peripheral Nerve Injury in Aged Mice

• Ashley Kalinski, Ph.D.
  Topic: Elucidating the cell-autonomy of SARM1 for injury induced axon regeneration, nerve inflammation, and Schwann cell reprogramming
• Atul Rawat, Ph.D.
  Topic: Modulating macrophage phenotype in peripheral nerve injury to accelerate nerve regeneration and functional recovery
• Baohan Pan, M.D., Ph.D.
  Topic: Cutaneous Sensory Innervation in Human and Mouse and Its Implications in Neuropathic Pain
• Christopher Cashman, Ph.D.
  Topic: Mitochondrial genome mutations and respiratory dysregulation as effectors of diabetic neuropathy
• Hyun Sung, Ph.D.
  Topic: Deciphering the role of autophagy in the pathogenesis of peripheral neuropathy
• Masnsen Cherief, Ph.D.
  Topic: Preventing diabetic bone disease using a neuroprotective agent
• Pabitra Sahoo, Ph.D.
  Topic: Establishing the kinetics for failure of axonal protein synthesis in chronic nerve injury
• Qin Zheng, M.D., Ph.D.
  Topic: In-vivo characterization of chemotherapy-induced neuropathy using large scale calcium imaging
• Simone Thomas, M.S.
  Topic: Chemotherapy-Induced Peripheral Neuropathy (CIPN) Assessment

• Sarah Berth, M.D., Ph.D.
  Topic: Genetic Screen for Axonal Degeneration Modifiers
• Aysel Fisgin, Ph.D.
  Topic: MAP4K4 Inhibition to Prevent CIPN
• Sang-Min Jeon, Ph.D.
  Topic: Sprouting Mediated Skin Reinnervation
• Ying Liu, M.D., Ph.D.
  Topic: Evaluating the effect of SARM1 deficiency on peripheral neuropathy in db/db mouse model of type 2 diabetes.
• Brett McCray, M.D., Ph.D.
  Topic: TRVP4 in Nerve Injury
• Kathryn Moss, Ph.D.
  Topic: Development of a CMT1A/CIPN Mouse Model
• Bipasha Mukherjee-Clavin, M.D., Ph.D.
  Topic: KIF16B-CMT2
• Seong-Hyun Park, Ph.D.
  Topic: CMT PNSorganoid Model
• Sami Tuffaha, M.D.
  Topic: Gene Expression Changes with Schwann Cell Denervation
• Eric Villalón Landeros, Ph.D.
  Topic: DRG Neuroproteasome Signaling Peptides

• LeeAnn Li, M.D., Ph.D.: Engineering an In Vitro Neuromuscular Model to Study Disease
• Cooper Hayes, M.D., Ph.D.: Decoding Diabetic Neuropathy via Spatial Transcriptomic Profiling of Human Dorsal Root Ganglia (DRG)
• Bipasha Mukherjee-Clavin, M.D., Ph.D.: Electron microscopy of early CMT1A peripheral nerves
• Bryce Chiang, M.D., Ph.D.: Direct current electrical stimulation of the optic nerve to stimulate nerve regeneration
• Yu Su, M.D., Ph.D. : Mechanistic investigation on the benefit of glutamate carboxypeptidase II (GCPII) inhibition in aging peripheral nerve injury (PNI) via spatial transcriptomics
• Mehmet Can Sari, M.D.: Single-Cell Transcriptomic Profiling of Human Sensory Neuron-like Cells (HC-1) During Early Differentiation

• Rachana Suresh, MBBS, MPH: Motor unit spatial distribution after reinnervation via nerve-to-nerve coaptation and direct neurotization
• Aysel Fisgin, Ph.D.: Identifying targets to prevent PIPN
• Sana Sarkar, Ph.D.: Single nuclei RNAseq of injured peripheral nerves lacking Schwann cell monocarboxylate transporters
• Chan-Hyun Na, Ph.D.: Identification of biomarkers for post-COVID19 onset POTS syndrome using proteomics approaches
• Mehmet Can Sari, M.D.: Exploring mRNA Methylation Dynamics Following Sciatic Nerve Injury in an In Vivo Model

• Guillermo Moya Alvarado, Ph.D. : Identifying membrane proteins delivered to axons by transcytosis
• Athanasios Alexandris, MBChB.: Identification of Genetic Modifiers of SARM1-mediated Neuronal Toxicity
• Tae Hwan Chung, M.D. : Investigating neuroaxonal injury markers for post-COVID syndrome with autonomic dysfunction.
• Weiran Chen, M.D. : Single cell RNA-seq to analyze the heterogeneity of cell clusters in hiPSC and hESC cultures differentiated towards satellite glia lineage
• Simone Thomas, MSc: Neurofilament Light Chain Plasma Levels in a Large Cohort of Patients with Idiopathic Polyneuropathy
• Sami Tuffaha, M.D.: Change in Glutamate Carboxypeptidase II Expression in Denervated and Reinnervated Muscles

• Bipasha Mukherjee-Clavin, M.D., Ph.D.: Modeling inherited neuropathies with human pluripotent stem cells
• Simone Thomas, MSc: Mobile EMG unit to perform nerve conduction testing with ICAVS study participants