Arens Taga, M.D., is a neurologist-scientist specializing in neuromuscular disorders. He earned his medical degree at the University of Parma, Italy, where he also completed a neurology residency. Dr. Taga subsequently moved to the United States to join Dr. Nicholas Maragakis’ laboratory at Johns Hopkins University as a research postdoctoral fellow. Following this, he completed a second neurology residency at Johns Hopkins Hospital and is currently pursuing advanced training as a neuromuscular fellow. His research focuses on utilizing human-induced pluripotent stem cells, multielectrode array recordings, and microfluidic devices to develop in vitro disease models and investigate the mechanisms of neurotoxicity and neuroprotection in Amyotrophic Lateral Sclerosis (ALS).

The fundamental biology of axonal regeneration, particularly in motor neurons, remains inadequately understood in human models. This knowledge gap limits the development of effective therapies for promoting nerve repair after injury and for treating neuropathies. A deeper understanding of motor axon biology is crucial for addressing the pathophysiology of motor neuron diseases like amyotrophic lateral sclerosis (ALS), where poor prognosis poses additional challenges. While recent studies in mouse and DRG cell models have shown that axonal protein synthesis, including β1-importin, is crucial for promoting axonal regeneration after mechanical injury, its role in human motor neurons is yet to be explored. This project seeks to elucidate the role of β1-importin in human motor axon regeneration by leveraging hiPSC-based models and microfluidic devices. The insights gained could lead to new approaches to enhance axonal regeneration for therapeutic purposes.

Dr. Athanasios Alexandris is a Research Associate in the Neuropathology division of the Department of Pathology at Johns Hopkins University School of Medicine. He earned his medical degree from the University of Leicester, UK, with an intercalated BSc in Neurosciences & Mental Health from Imperial College London. During his medical training, he conducted neuropathology research with the Neurodegenerative Pathology Research Group at Newcastle University and later pursued postdoctoral research at Johns Hopkins in the laboratory of Dr. Vassilis E. Koliatsos, where he integrated experimental neuropathology with advanced cellular and molecular techniques to investigate axonal injury and repair mechanisms in both in vitro and in vivo models.

His current research focuses on understanding molecular pathways related to axonal degeneration and maintenance in the context of injury and neurodegenerative disease models, as well as exploring the role of axonal plasticity in the adult central nervous system in neurological recovery following injury.

This project investigates how a newly identified protein modulates the activity of SARM1, an enzyme critical for axonal degeneration in neurological diseases such as peripheral neuropathies. Building on a recent genetic screen, Dr. Athanasios Alexandris and Dr. Zhe Zhang identified candidate regulators of SARM1 activity, including one whose knockdown effectively prevents SARM1 activation and axon destruction. Supported by the Merkin PNNR seed grant, the team will conduct in-depth experiments to understand how this modulation impacts SARM1-driven neurotoxicity in disease-relevant in vitro and in vivo models. They aim to elucidate the mechanisms underlying this regulation, validate findings across diverse systems, and lay the groundwork for developing innovative therapeutic strategies for neurodegenerative diseases.

Dr. Bipasha Mukherjee-Clavin is an Assistant Professor of Neurology and co-Director of the Johns Hopkins CMT clinic.  She completed her M.D./Ph.D. degrees, Neurology residency, and clinical Neuromuscular fellowship in the Johns Hopkins University School of Medicine.  She joined the Johns Hopkins Neurology faculty as an Assistant Professor in 2022.  She is committed to understanding the biology of common, genetic demyelinating neuropathies like CMT1A so that rational treatments can be developed.

CMT1A is a common genetic demyelinating peripheral neuropathy caused by PMP22 duplication that currently lacks disease modifying treatments. It is currently unclear when in Schwann cell development CMT1A pathology emerges and how the PMP22 duplication results in Schwann cell dysfunction.  Here we proposed using single cell RNA sequencing on sciatic nerves of a well validated humanized CMT1A mouse model (C3 mouse) at three early developmental time points to learn when molecular evidence of Schwann cell dysfunction first emerges in CMT1A and also to identify putative mechanisms. 

Diana Tavares Ferreira holds a PharmD/MS from the University of Coimbra (Portugal) and completed her Ph.D. in Neuroscience at the University of Sheffield (UK), followed by a postdoctoral fellowship at UT Dallas (US). In 2022, she received the Peter J. Dyck Abstract Award for Diabetic Neuropathy Research from the Peripheral Nerve Society. In January 2024, Diana began her role as an Assistant Professor of Neuroscience at UT Dallas. Her research focuses on axonal transport and RNA regulation in neurodegeneration and peripheral neuropathies, employing a range of omics and computational approaches.

Diabetic peripheral neuropathy (DPN) is one of the most common and debilitating outcomes of diabetes and the most common cause of neuropathy. DPN is caused by pathological changes in the distal axons of sensory neurons, which are highly polarized cells with axons emanating from the dorsal root ganglion (DRG). This highlights the importance of axon integrity as a mechanism of clinical features of DPN. This project aims to investigate the molecular mechanisms underlying axonal degeneration in DPN. Our research aims to understand how disruptions in messenger RNA (mRNA) transport within peripheral nerves contribute to nerve degeneration. mRNA transport is important because it allows cells, including neurons, to produce the proteins at the right place and time, which is essential for proper nerve function. By mapping how specific mRNAs are transported in nerve cells from people with and without diabetic peripheral neuropathy, we hope to uncover new insights that could lead to personalized treatments for this condition, which currently lacks tailored therapies.

Patricia Jillian Ward, Ph.D., is an Assistant Professor in the Department of Cell Biology at Emory University School of Medicine. She serves on the Scientific Advisory Board for The International Symposium for Neural Regeneration and the steering committee for the NIH Common Data Elements in Preclinical Spinal Cord Injury Research. She is a member of the National Neurotrauma Society, the American Association of Anatomy, and the Society for Neuroscience, and serves as a council member for the Atlanta Chapter of the Society for Neuroscience. Dr. Ward is also affiliated with Emory’s Neuroscience Graduate Program and the Genetics and Molecular Biology Graduate Program. She earned her B.S. in Animal Sciences from Auburn University, graduating summa cum laude as a Bryant-Jordan Student-Athlete Fellow. She completed her Ph.D. in Anatomical Sciences and Neurobiology at the University of Louisville, supported by an NIH NRSA F31 fellowship, where she studied the effects of treadmill locomotor training on spinal cord injury outcomes in rats. Her postdoctoral research at Emory, funded by an NIH NRSA F32 fellowship, focused on enhancing peripheral axon regeneration through exercise, optogenetics, and electrical stimulation, emphasizing sex differences in transgenic models. Dr. Ward has been recognized with an Early Career Research Award from NIH/NICHD and the R.R. Bensley Early-Career Investigator Award in Cell Biology.

A critical knowledge gap in neuroscience is the purpose of sympathetic signaling at the neuromuscular junction, how sympathetic axons associated with neuromuscular junctions respond to nerve injuries and what their contribution is to functional recovery or dysfunction. Our most recent work using a sympathetic-specific ablation revealed that muscle mitochondrial metabolism is modulated by sympathetic innervation despite the retention of motor and sensory innervation. Muscle mitochondria that lack sympathetic signaling lose the ability to metabolize long-chain fatty acids (LCFA). LCFA disorders are well-known to be characterized by muscle weakness and early muscle fatigue. Our novel finding emphasizes the importance of functional sympathetic axon regeneration in the context of nerve injury, and importantly muscle fatigue is a clinically relevant characteristic of reinnervated muscle.

Our preliminary data indicate that many sympathetic axons in the sciatic nerve do not elongate after nerve transection. Furthermore, we find that treatments known to modestly promote motor and sensory regeneration inhibit the number of sympathetic neurons participating in regeneration. In this study, our group will test the hypothesis that failure of sympathetic reinnervation to muscle contributes to mitochondrial dysfunction and muscle fatigue following peripheral nerve injury and is an impediment to functional recovery after nerve injury.

Dr. Jorge Gomez Deza is an Assistant Professor in the Department of Cancer and Cellular Biology at the Lewis Katz School of Medicine, Temple University. He earned his Ph.D. in the laboratory of Dr. Chris Shaw, studying amyotrophic lateral sclerosis (ALS). Following this, he joined the NIH under the mentorship of Dr. Claire Le Pichon, focusing on the effects of axon injury and chemotherapy on human neurons.

Currently, Dr. Gomez Deza's team centers on understanding the molecular mechanisms through which chemotherapy induces neuronal damage. His team employs iPSC-derived neurons and takes an unbiased multiomic approach. They integrate whole-genome CRISPRi screens, RNA-seq, and high-throughput confocal microscopy to identify new mechanisms of neuron injury. The lab maintains a strong clinical focus, with a deep commitment to uncovering novel molecular pathways driving axon degeneration and neuronal death. Their ultimate goal is to develop innovative therapeutic strategies to combat chemotherapy-induced neuronal damage.

The goal of this project is to identify novel, clinically relevant targets for treating chemotherapy-induced peripheral neuropathy (CIPN). While vincristine is essential for cancer treatment, it frequently causes CIPN, often leading to dose reduction or treatment discontinuation, thereby negatively impacting treatment outcomes.

We previously conducted the first whole-genome CRISPRi screen to identify drivers of vincristine-induced neuronal. Many of the identified genes modulate apoptosis, and silencing these hits may interfere with the efficacy of chemotherapy. We hypothesize that targeting non-essential genes could mitigate CIPN while minimizing side effects.

In this project, we will investigate the effects of silencing non-essential gene candidates on preventing vincristine-induced axon degeneration in mature human sensory neurons. Additionally, we will validate that silencing these genes does not promote cancer cell proliferation in vitro. By employing an unbiased approach, we aim to gain a deeper understanding of the molecular mechanisms underlying axon degeneration and to identify novel therapeutic targets for CIPN that do not compromise the efficacy of chemotherapy.

Throughout my academic training and research in Algeria and France, I had the chance to develop my scientific background in several disciplines including molecular biology, histology, microscopy, and radiography. My engineering training in Algeria was oriented towards food industry.

I moved to Baltimore in 2019, As a postdoctoral fellow at the James lab, my research interests include perivascular mesenchymal progenitor cells for osteoarthritis repair and the study of the peripheral nervous system and its importance in bone and tendon tissue repair. 

We recently described two perivascular mesenchymal cells subtypes (Pdgfrα+ and Pdgfrβ+) that improved murine osteoarthritis. Pdgfrα+ and Pdgfrβ+ cell preparations improved metrics of cartilage degradation and reduced markers of chondrocyte hypertrophy in a mice osteoarthritis model (5).  

One of my interests, is studying the role of peripheral nervous system in bone and tendon. I'm working on developing a better understanding to the link between diabetic neuropathy and diabetic bone disease using omnics, histology and µCT data.

The primary objectives of this project are two-fold. First, we aim to reconstruct peripheral nerve-to-metatarsal interactions in silico, under both diabetic and non-diabetic conditions. This will elucidate the neuro-skeletal communication networks affected by diabetes. Second, we intend to assess the efficacy of a near-clinical small molecule neuroprotective agent, NB-3, in preventing diabetic bone disease. By achieving these objectives, we aim to bridge the gap between symptom management and disease prevention in diabetic patients.