Cervical myelopathy is part of ALS mimic syndrome and should be considered in patients with clinical signs of motor neuron disease.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7981701 | PMC |
| http://dx.doi.org/10.1002/ccr3.3740 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Gain-of-function ANXA11 mutation cause late-onset ALS with aberrant protein aggregation, neuroinflammation and autophagy impairment.
Acta Neuropathol Commun
January 2025
Department of Neurology, Peking Union Medical College Hospital, Peking Union Medical College (PUMC) and Chinese Academy of Medical Science (CAMS), Beijing, China.
Mutations in the ANXA11 gene, encoding an RNA-binding protein, have been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS), but the underlying in vivo mechanisms remain unclear. This study examines the clinical features of ALS patients harboring the ANXA11 hotspot mutation p.P36R, characterized by late-onset motor neuron disease and occasional multi-system involvement.
View Article and Find Full Text PDFToxic effects and mechanistic insights of cadmium telluride quantum dots on the homeostasis and regeneration in planarians.
J Hazard Mater
December 2024
College of Life Science, Henan Normal University, Xinxiang 453007, China. Electronic address:
The widespread application of quantum dots (QDs) in recent years has raised concerns about potential environmental and human health risks. Although the toxicity of cadmium telluride quantum dots (CdTe QDs) has been partially studied, their effects on stem cells, tissue regeneration, neurodevelopment, and neurobehavioral toxicity remain unclear. This study aimed to investigate the combined toxic effects and mechanisms of CdTe QDs on planarians at the individual, tissue, cellular, and molecular levels.
View Article and Find Full Text PDFMagnetic field-oriented conductive decellularized extracellular matrix hydrogel synergizes with electrical stimulation to promote spinal cord injury repair and electrophysiological function restoration.
Biomater Adv
December 2024
Key Laboratory for Ultrafine Materials of Ministry of Education, Frontiers Science Center for Materiobiology and Dynamic Chemistry, Engineering Research Center of Biomedical Materials of Ministry of Education, School of Materials Science and Engineering, East China University of Science and Technology, Shanghai 200237, PR China. Electronic address:
Spinal cord injury (SCI) results in electrophysiological and behavioral dysfunction. Electrical stimulation (ES) is considered to be an effective treatment for mild SCI; however, ES is not applicable to severe SCI due to the disruption of electrical conduction caused by tissue defects. Therefore, the use of conductive materials to fill the defects and restore electrical conduction in the spinal cord is a promising therapeutic strategy.
View Article and Find Full Text PDFAutosomal-recessive spastic ataxia of Charlevoix-Saguenay (ARSACS) is an early-onset neurodegenerative disease caused by mutations in the SACS gene. The first two mutations were identified in French Canadian populations 20 years ago. The disease is now known as one of the most frequent recessive ataxias worldwide.
View Article and Find Full Text PDFVimentin Inhibits Neuronal Apoptosis After Spinal Cord Injury by Enhancing Autophagy.
CNS Neurosci Ther
January 2025
Dongguan Key Laboratory of Stem Cell and Regenerative Tissue Engineering, the First Dongguan Affiliated Hospital, School of Basic Medical Sciences, Guangdong Medical University, Dongguan, China.
Aims: Neuron death is caused primarily by apoptosis after spinal cord injury (SCI). Autophagy, as a cellular response, can maintain cellular homeostasis to reduce apoptosis. We aimed to investigate the effect and the mechanism of vimentin knockdown on autophagy and neural recovery after SCI.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!