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Tail Anchored protein insertion mediated by CAML and TRC40 links to neuromuscular function in mice.
PLoS Genet
January 2025
Department of Pediatric and Adolescent Medicine, Mayo Clinic, 200 1st St. SW, Rochester, Minnesota 55905, United States of America.
Motor neuron diseases, such as amyotrophic lateral sclerosis (ALS) and progressive bulbar palsy, involve loss of muscle control resulting from death of motor neurons. Although the exact pathogenesis of these syndromes remains elusive, many are caused by genetically inherited mutations. Thus, it is valuable to identify additional genes that can impact motor neuron survival and function.
View Article and Find Full Text PDFCemdomespib Therapy Slows the Progression of Neuromuscular Weakness and Demyelination in the R75W-Connexin 32 Animal Model of Charcot-Marie-Tooth 1X Disease.
ACS Pharmacol Transl Sci
January 2025
Department of Pharmacology and Toxicology, University of Kansas, Lawrence, Kansas 66045, United States.
Mutations in connexin 32 (Cx32) are a common cause of Charcot-Marie-Tooth 1X (CMT1X) disease, an inherited peripheral neuropathy characterized by progressive neuromuscular weakness and demyelination. There are no approved pharmacologic therapies for CMT1X, and identifying new treatments that slow the onset and severity of neuromuscular decline may aid disease management. Cemdomespib is an orally bioavailable small molecule that improved demyelination and neuromuscular junction (NMJ) morphology in mice lacking Cx32 expression.
View Article and Find Full Text PDFMyasthenia Gravis as a Paraneoplastic Manifestation of Renal Cell Carcinoma: More Than a Coincidence?
Ann Neurosci
January 2025
Department of Neurology, Pushpagiri Institute of Medical Sciences and Research Centre, Thiruvalla, Kerala, India.
Background: Myasthenia gravis is an autoimmune neuromuscular disease primarily caused by autoantibodies against nicotinic acetylcholine receptors (AChRs) at the neuromuscular junction. However, extrathymic malignancies need to be considered in the elderly population.
Purpose: Although thymic malignancy is the most common tumour association, several extrathymic malignancies complicated with myasthenia gravis have been reported.
Local Inflammation Precedes Diaphragm Wasting and Fibrotic Remodelling in a Mouse Model of Pancreatic Cancer.
J Cachexia Sarcopenia Muscle
February 2025
Department of Physical Therapy, University of Florida Health Cancer Center, Gainesville, Florida, USA.
Background: Cancer cachexia represents a debilitating muscle wasting condition that is highly prevalent in gastrointestinal cancers, including pancreatic ductal adenocarcinoma (PDAC). Cachexia is estimated to contribute to ~30% of cancer-related deaths, with deterioration of respiratory muscles suspected to be a key contributor to cachexia-associated morbidity and mortality. In recent studies, we identified fibrotic remodelling of respiratory accessory muscles as a key feature of human PDAC cachexia.
View Article and Find Full Text PDFMitochondrial Complex I and ROS control synapse function through opposing pre- and postsynaptic mechanisms.
bioRxiv
December 2024
Department of Anatomy and Cell Biology, University of Iowa Carver College of Medicine, Iowa City, IA, 52242, USA.
Neurons require high amounts energy, and mitochondria help to fulfill this requirement. Dysfunctional mitochondria trigger problems in various neuronal tasks. Using the neuromuscular junction (NMJ) as a model synapse, we previously reported that Mitochondrial Complex I (MCI) subunits were required for maintaining NMJ function and growth.
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