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There are several CMT2D mouse models, but\n                  <jats:italic>Gars<\/jats:italic>\n                  <jats:sup>\n                    \u0394\n                    <jats:italic>ETAQ<\/jats:italic>\n                    \/+\n                  <\/jats:sup>\n                  is the only one that bears a patient-sourced mutation. Created using CRISPR\/Cas9 to model a 12-nucleotide\n                  <jats:italic>de novo GARS1<\/jats:italic>\n                  deletion identified in an unusually severe CMT2D patient,\n                  <jats:italic>Gars<\/jats:italic>\n                  <jats:sup>\n                    <jats:italic>\u0394<\/jats:italic>\n                    ETAQ\n                    <jats:italic>\/+<\/jats:italic>\n                  <\/jats:sup>\n                  mice have previously been shown to display several neuromuscular phenotypes; motor axon loss, denervated neuromuscular junctions (NMJs) and reduced muscle function. Here, we extend these analyses to provide a more comprehensive understanding of both motor and sensory nerve deficits across hind- and fore-limbs. At 3 months,\n                  <jats:italic>Gars<\/jats:italic>\n                  <jats:sup>\n                    \u0394\n                    <jats:italic>ETAQ<\/jats:italic>\n                    \/+\n                  <\/jats:sup>\n                  mice possess sex-independent alterations in the levels of neuropathy biomarkers \u2013 including decreased NfL and increased periaxin \u2013 alongside reduced muscle endurance and strength, and impairments in the sensory modalities of mechanosensation, proprioception and nociception. Underpinning these dysfunctions, we identified site-specific defects comprising altered sensory neuron populations, muscle spindle loss, reduced motor neuron size, disrupted NMJ innervation and maturation, and reduced axonal transport of signalling endosomes\n                  <jats:italic>in vivo<\/jats:italic>\n                  . Together, these experiments show that\n                  <jats:italic>Gars<\/jats:italic>\n                  <jats:sup>\n                    \u0394\n                    <jats:italic>ETAQ<\/jats:italic>\n                    \/+\n                  <\/jats:sup>\n                  mice display robust and selective peripheral nerve pathology that manifests in a general distal-to-proximal fashion, priming this CMT2D allele for testing treatments and evaluating mechanisms underlying peripheral nerve vulnerability.\n                <\/jats:p>\n                <jats:sec>\n                  <jats:title>Abstract Figure<\/jats:title>\n                  <jats:fig id=\"ufig1\" position=\"float\" fig-type=\"figure\" orientation=\"portrait\">\n                    <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"736541v1_ufig1\" position=\"float\" orientation=\"portrait\"\/>\n                  <\/jats:fig>\n                <\/jats:sec>","DOI":"10.64898\/2026.07.05.736541","type":"posted-content","created":{"date-parts":[[2026,7,10]],"date-time":"2026-07-10T00:00:11Z","timestamp":1783641611000},"source":"Crossref","is-referenced-by-count":0,"title":["The neuropathy-causing\n                  <i>GARS1<\/i>\n                  <sup>\n                    \u0394\n                    <i>ETAQ<\/i>\n                  <\/sup>\n                  mutation drives pathology in subsets of motor and sensory neurons in mice"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8093-2139","authenticated-orcid":false,"given":"Rebecca L.","family":"Simkin","sequence":"first","affiliation":[{"name":"Department of Neuromuscular Diseases, UCL Queen Square Institute of Neurology, University College London, London, UK"},{"name":"UCL Queen Square Motor Neuron Disease Centre, UCL Queen Square Institute of Neurology, University College London, London, UK"},{"name":"The Francis Crick Institute, London, 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