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Neurological disorders are prevalent in horses, but their study is challenging due to anatomic constraints and the large body size; very few host-specific in vitro models have been established to study these types of diseases, particularly from adult donor tissue. Here we report the generation of primary neuronal dorsal root ganglia (DRG) cultures from adult horses: the mixed, dissociated cultures, containing neurons and glial cells, remained viable for at least 90 days. Similar to DRG neurons in vivo, cultured neurons varied in size, and they developed long neurites. The mitochondrial movement was detected in cultured cells and was significantly slower in glial cells compared to DRG-derived neurons. In addition, mitochondria were more elongated in glial cells than those in neurons. Our culture model will be a useful tool to study the contribution of axonal transport defects to specific neurodegenerative diseases in horses as well as comparative studies aimed at evaluating species-specific differences in axonal transport and survival.
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http://dx.doi.org/10.1111/joa.13719 | DOI Listing |
Charcot-Marie-Tooth disease (CMT) is an inherited peripheral neuropathy characterized by sensory dysfunction and muscle weakness, manifesting in the most distal limbs first and progressing more proximal. Over a hundred genes are currently linked to CMT with enrichment for activities in myelination, axon transport, and protein synthesis. Mutations in tRNA synthetases cause dominantly inherited forms of CMT and animal models with CMT-linked mutations in these enzymes display defects in neuronal protein synthesis.
View Article and Find Full Text PDFACS Chem Neurosci
September 2025
College of Pharmacy, Gachon Institute of Pharmaceutical Science, Gachon University, Incheon 21912, Republic of Korea.
Neurological disorders such as Alzheimer's Disease, Parkinson's Disease, Huntington's Disease, Multiple Sclerosis, and Amyotrophic Lateral Sclerosis pose significant challenges for treatment. Reasons for the difficulty in finding cures for these conditions include complications in early diagnosis, progressive and irreversible neuronal damage, and the presence of the blood-brain barrier (BBB), which hinders the delivery of drugs to the affected areas of the brain. Intranasal (INL) drug administration has increasingly gained popularity among researchers for targeting neurological conditions, because of its ability to bypass the BBB.
View Article and Find Full Text PDFFront Neurosci
August 2025
School of Biology, Manchester Academic Health Science Centre, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, United Kingdom.
Mitochondrial dysfunction is an important cause for neurodegeneration, often associated with dyshomeostasis of reactive oxygen species, i.e., oxidative stress.
View Article and Find Full Text PDFNeural Regen Res
September 2025
College of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine, Hefei, Anhui Province, China.
Neurodegenerative disorders are typically caused by harmful protein accumulation and nerve cell damage. A post-translational modification called O-linked N-acetylglucosamine ylation acts as a critical regulator in these disorders by controlling protein behavior, cell signaling, and energy balance. This modification is dynamically balanced through the cooperative actions of O-linked N-acetylglucosamine transferase and O-GlcNAcase.
View Article and Find Full Text PDFBr J Pharmacol
September 2025
Department of Pharmacy, Birla Institute of Technology and Science (BITS), Pilani - Hyderabad Campus, Hyderabad, India.
Peripheral neuropathic pain, arising from peripheral nerve injuries, remains a significant clinical challenge because of complex pathophysiology and limited treatment options. Conventional treatments primarily provide symptomatic relief, failing to address underlying nerve damage. The extracellular matrix (ECM) plays a vital role in nerve regeneration by offering structural support and biochemical signals that regulate Schwann cell behaviour, axonal growth and microenvironment remodelling.
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