Axons are processes of neurons, up to a metre long, that form the essential biological cables wiring nervous systems. They must survive, often far away from their cell bodies and up to a century in humans. This requires self-sufficient cell biology including structural proteins, organelles, and membrane trafficking, metabolic, signalling, translational, chaperone, and degradation machinery-all maintaining the homeostasis of energy, lipids, proteins, and signalling networks including reactive oxygen species and calcium. Axon maintenance also involves specialised cytoskeleton including the cortical actin-spectrin corset, and bundles of microtubules that provide the highways for motor-driven transport of components and organelles for virtually all the above-mentioned processes. Here, we aim to provide a conceptual overview of key aspects of axon biology and physiology, and the homeostatic networks they form. This homeostasis can be derailed, causing axonopathies through processes of ageing, trauma, poisoning, inflammation or genetic mutations. To illustrate which malfunctions of organelles or cell biological processes can lead to axonopathies, we focus on axonopathy-linked subcellular defects caused by genetic mutations. Based on these descriptions and backed up by our comprehensive data mining of genes linked to neural disorders, we describe the 'dependency cycle of local axon homeostasis' as an integrative model to explain why very different causes can trigger very similar axonopathies, providing new ideas that can drive the quest for strategies able to battle these devastating diseases.
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http://dx.doi.org/10.3389/fnins.2023.1236815 | DOI Listing |
Heliyon
January 2025
Department of Biomolecular Sciences, University of Urbino Carlo Bo, Urbino, Italy.
Compelling evidence has demonstrated that rehabilitation through physical exercise, a non-invasive and non-surgical intervention, enhances muscle reinnervation and motor recovery after peripheral nerve injury (PNI) by increasing muscle-derived brain-derived neurotrophic factor (BDNF) expression and triggering TrkB-dependent axonal plasticity. Adenosine has been widely acknowledged to trigger TrkB via A2A receptor (A2AR). Since motor nerve terminals co-express TrkBs and A2ARs and depolarizing conditions increase muscle release of BDNF and adenosine, we examined whether A2ARs activation could recapitulate the functional recovery benefits of intermittent exercise after a nerve crush.
View Article and Find Full Text PDFCancer Metastasis Rev
January 2025
Cancer Early Detection Advanced Research Center (CEDAR), Knight Cancer Institute, Oregon Health and Science University, Portland, OR, USA.
Nerve signaling within the tumor microenvironment (TME) plays a critical role in the initiation, progression, and metastasis of solid tumors. Due to their highly responsive behavior and activation upon injury and cancer onset, this review specifically focuses on how sympathetic nerves rewire the TME. Within tumors, sympathetic nerves closely interact with various TME components, and their combined signaling often shifts tumor-intrinsic physiology toward tumor-supportive phenotypes.
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 PDFASN Neuro
January 2025
Department of Cell & Developmental Biology, SUNY Upstate Medical University, Syracuse, NY, USA.
Functional recovery following spinal cord injury will require the regeneration and repair of damaged neuronal pathways. It is well known that the tissue response to injury involves inflammation and the formation of a glial scar at the lesion site, which significantly impairs the capacity for neuronal regeneration and functional recovery. There are initial attempts by both supraspinal and intraspinal neurons to regenerate damaged axons, often influenced by the neighboring tissue pathology.
View Article and Find Full Text PDFJ Orthop Res
January 2025
Department of Orthopaedic Surgery, Montefiore Einstein, Bronx, New York, USA.
Compression neuropathy is a prevalent medical condition, including common types such as carpal tunnel syndrome, cubital tunnel syndrome, sciatica, and many others. While the neurological consequences are well understood, the effects on bone properties and the potential downstream impact on fracture risk remain less clear. This study aimed to assess the influence of compressive neuropathy on bone properties using a rabbit model of sciatic nerve compression.
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