Diabetes mellitus is a chronic disease with numerous complications that severely impact on the quality of life of patients. Different neuropathies may arise as complications associated with the nervous system, both peripherally and at the central level. The mechanisms behind these neuronal complications are far from being clarified, but axonal transport impairment, a vital process for neuronal physiology, has been described in the context of experimental diabetes. Alterations in neuronal cytoskeleton and motor proteins, deficits in ATP supply or neuroinflammation, as processes that disturb the effective transport of cargoes along the axon, were reported as putative causes of axonal impairment, ultimately leading to axonal degeneration. The main goal of the present review is to reunite the main studies in the literature exploring diabetes-induced alterations likely involved in axonal transport deficits, and call the attention for the uttermost importance of further exploring the field. Understanding the mechanisms underlying neuronal deficits in diabetes is crucial for the development of new therapeutic strategies to prevent neuronal degeneration in diabetes and related neuropathies.
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http://dx.doi.org/10.1007/s12035-018-1227-1 | DOI Listing |
Rev Physiol Biochem Pharmacol
January 2025
Institute of Medical Sciences, University of Aberdeen, Aberdeen, Scotland, UK.
Pre- and post-synaptic events are regulated by liquid-liquid phase separation and this phenomenon requires multiple electrical forces. Both axonal transport and the organization of postsynaptic excitatory and inhibitory receptors are regulated by LLPS, with its mandatory electrical drivers ultimately determining our cognitive health and capacity.
View Article and Find Full Text PDFJCI Insight
January 2025
Gavin Herbert Eye Institute-Center for Translational Vision Research, Depar, University of California Irvine School of Medicine, Irvine, United States of America.
Elevation of intraocular pressure (IOP) due to trabecular meshwork (TM) dysfunction, leading to neurodegeneration, is the pathological hallmark of primary open-angle glaucoma (POAG). Impaired axonal transport is an early and critical feature of glaucomatous neurodegeneration. However, a robust mouse model that accurately replicates these human POAG features has been lacking.
View Article and Find Full Text PDFInt J Ophthalmol
January 2025
Department of Ophthalmology, the Second Affiliated Hospital of Xi'an Medical University, Xi'an 710038, Shaanxi Province, China.
Glaucoma is a group of diseases characterized by progressive optic nerve degeneration, with the characteristic pathological change being death of retinal ganglion cells (RGCs), which ultimately causes visual field loss and irreversible blindness. Elevated intraocular pressure (IOP) remains the most important risk factor for glaucoma, but the exact mechanism responsible for the death of RGCs is currently unknown. Neurotrophic factor deficiency, impaired mitochondrial structure and function, disrupted axonal transport, disturbed Ca homeostasis, and activation of apoptotic and autophagic pathways play important roles in RGC death in glaucoma.
View Article and Find Full Text PDFNeurochem Int
January 2025
Department of Neurology, Osaka University Graduate School of Medicine, Osaka, Japan; Department of Neurotherapeutics, Osaka University Graduate School of Medicine, Osaka, Japan; Mount Fuji Research Institute, Yamanashi Prefectural Government, Yamanashi, Japan. Electronic address:
Amyotrophic lateral sclerosis (ALS) is characterized by the mislocalization and abnormal deposition of TAR DNA-binding protein 43 (TDP-43). This protein plays important roles in RNA metabolism and transport in motor neurons and glial cells. In addition, abnormal iron accumulation and oxidative stress are observed in the brain and spinal cord of patients with ALS exhibiting TDP-43 pathology and in animal models of ALS.
View Article and Find Full Text PDFJ Neurol
January 2025
Centre de Génétique Humaine, Centre Hospitalier Universitaire de Besançon, Besançon, France.
Introduction: The MAPT gene encodes Tau, a protein mainly expressed by neurons. Tau protein plays an important role in cerebral microtubule polymerization and stabilization, in axonal transport and synaptic plasticity. Heterozygous pathogenic variation in MAPT are involved in a spectrum of autosomal dominant neurodegenerative diseases known as taupathies, including Alzheimer's disease, Pick's disease, fronto-temporal dementia, cortico-basal degeneration and progressive supranuclear palsy.
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