Lab Members

Dr. Conrad “Chris” Weihl MD/PhD is a Professor of Neurology and Head of the Neuromuscular Section at Washington University School of Medicine in St. Louis, Missouri, USA. He received his MD and PhD from the University of Chicago Pritzker School of Medicine followed by a Neurology Residency and Neuromuscular Fellowship at Washington University.  During his post-doctoral fellowship, he began to study the molecular pathogenesis of hereditary inclusion body myopathies and now has an active clinical and basic science research program focused on genetics, protein aggregate myopathies, inclusion body myositis and limb-girdle muscular dystrophies.  His research has delineated the molecular mechanism of VCP associated inclusion body myopathy and identified the genetic cause of LGMDD1.  He has received a number of honors including the Derek Denny-Brown Young Neurological Scholar Award from the American Neurological Association and the inaugural Daniel and Jephta Drachman Family Award from Johns Hopkins University.  He is currently a member of the WMS meeting planning committee and past-chair of the ANA scientific program advisory committee.  He is an active member ClinGen Neuromuscular Working Group and Chair of the ClinGen LGMD gene and variant curation expert panels.  Dr. Weihl has a strong commitment to the training of future neuromuscular clinicians and myologists.  He was awarded a K24 mid-career investigator award to mentor residents, fellows, junior faculy and early stage scientists in patient oriented research.  In his free time he enjoys listening to live music and spending time with his wife and two sons.

Chengcheng’s research interest is to develop new high-throughput approaches to functionally screen missense variants in LGMD-related genes. As an example, in order to link the sequence of each SGCA variant to its functional capacity (proper membrane localization), they established a FACS-based assay which is able to identify SGCA variants which fail to properly localize to the cell membrane. Reclassifying variants of unknown significance would broaden the spectrum of putative disease-causing variants, helping improve the LGMD-2D diagnosis, allow wider use of gene therapy, and enable new treatment design.

Muscular dystrophies are a disabling and often fatal form of hereditary muscle disease. No proven therapies exist for many forms. Dr. Ibaceta’s research has been focused on the characterization of molecular pathways involved in the development of neuromuscular disorders linked to mutations in protein chaperones DNAJB6 and DNAJB4. Her studies explore not only the pathogenesis of these neuromuscular disorders but also the identification of new strategies for the treatment of these diseases based mainly on mouse models and primary cultures.

Eileen received her B.S. in Biomedical Engineering from Rensselaer Polytechnic Institute in Troy, NY and her Ph.D. in Cellular and Molecular Pathology from University of Wisconsin-Madison. As a postdoc in the Weihl lab she studies TDP-43 aggregation in skeletal muscle. Her focus is on prion-like seeding of aggregates and how mutations in VCP can lead to TDP-43 aggregation in both skeletal muscle and neural tissue. In her free time Eileen loves attending concerts and running.

Michio is a pediatric neurologist with a deep interest in protein aggregate myopathy and protein homeostasis. He earned his PhD under the guidance of Dr. Ichizo Nishino at the National Center of Neurology and Psychiatry in Japan, focusing his research on genetic and inflammatory muscle diseases. Currently, Michio’s work is centered on unraveling the role of DNAJ proteins in muscle diseases, contributing to the broader understanding and potential treatment strategies in this field.

Munenori has studied patients with myopathy and he is deeply interested in inclusion body myopathy. Munenori’s work centers on defining lysosomal damage and lysosomal function following protopathic aggregate uptake in skeletal muscle, contributing to the broader understanding of lysosomal damage seen in inclusion body myopathy.