Three-dimensional (3D) printers mainly create 3D objects by stacking thin layers of material. The effect of the tools created using the fused deposition modeling (FDM) 3D printer on nerve cells remains unclear. In this study, the effects of polytetrafluoroethylene (PTFE) models and two different types of polylactic acid (PLA) models (white or natural), were created using the FDM 3D printer on axon extension were compared using the Campenot chamber. Neurons were isolated from the dorsal root ganglia and added to the central compartment of the Campenot chambers after isolation, processing, and culturing. On day 7, after the initiation of the culture, the difference of the axon extensions to the side compartments of each group was confirmed. We also compared the pH and the amount of leakage when each of these chambers was used. The PLA was associated with a shorter axon extension than the PTFE (white = 0.0078, natural = 0.00391). No difference in the pH was observed ( = 0.347), but there was a significant difference on multiple group comparison ( = 0.0231) in the amount of leakage of the medium. PTFE was found to be a more suitable material for culturing attachments.
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http://dx.doi.org/10.1515/biol-2022-0031 | DOI Listing |
Muscle Nerve
January 2025
Service ENMG et de Pathologies Neuromusculaires, Centre de référence Des Maladies Neuromusculaires PACA-Réunion-Rhône Alpes, Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Bron, France.
Introduction/aims: Finger Extension Weakness and DOwnbeat Nystagmus Motor Neuron Disease (FEWDON-MND) is characterized by motor weakness predominantly affecting finger extension, accompanied by downbeat nystagmus. To date, only 11 patients have been reported. The present study adds a further three and aims to provide a more detailed description of the electrodiagnostic features of these patients.
View Article and Find Full Text PDFPLoS Genet
January 2025
Department of Molecular Biosciences, Program in Molecular, Cellular, and Developmental Biology, KU Center for Genomics, University of Kansas, Lawrence, Kansas, United States of America.
Recent studies in vertebrates and Caenorhabditis elegans have reshaped models of how the axon guidance cue UNC-6/Netrin functions in dorsal-ventral axon guidance, which was traditionally thought to form a ventral-to-dorsal concentration gradient that was actively sensed by growing axons. In the vertebrate spinal cord, floorplate Netrin1 was shown to be largely dispensable for ventral commissural growth. Rather, short range interactions with Netrin1 on the ventricular zone radial glial stem cells was shown to guide ventral commissural axon growth.
View Article and Find Full Text PDFJ Prev Alzheimers Dis
January 2025
Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, Arizona, USA. Electronic address:
Background: There are no approved oral disease-modifying treatments for Alzheimer's disease (AD).
Objectives: The objective of this study was to assess efficacy and safety of blarcamesine (ANAVEX®2-73), an orally available small-molecule activator of the sigma-1 receptor (SIGMAR1) in early AD through restoration of cellular homeostasis including autophagy enhancement.
Design: ANAVEX2-73-AD-004 was a randomized, double-blind, placebo-controlled, 48-week Phase IIb/III trial.
Neuroinformatics
January 2025
Blue Brain Project, EPFL, Chemin des mines 9, 1202, Geneva, Switzerland.
Long-range axons are fundamental to brain connectivity and functional organization, enabling communication between different brain regions. Recent advances in experimental techniques have yielded a substantial number of whole-brain axonal reconstructions. While previous computational generative models of neurons have predominantly focused on dendrites, generating realistic axonal morphologies is more challenging due to their distinct targeting.
View Article and Find Full Text PDFAlzheimers Res Ther
January 2025
Alzheimer Center Amsterdam, Department of Neurology, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, The Netherlands.
Background: Disease-modifying therapies targeting the diverse pathophysiology of Alzheimer's disease (AD), including neuroinflammation, represent potentially important and novel approaches. The glucagon-like peptide-1 receptor agonist semaglutide is approved for the treatment of type 2 diabetes and obesity and has an established safety profile. Semaglutide may have a disease-modifying, neuroprotective effect in AD through multimodal mechanisms including neuroinflammatory, vascular, and other AD-related processes.
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