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The pathological hallmarks of the disease are defined by selective loss of spinal and bulbar motor neurons, accompanied by weakness, atrophy and fasciculations of bulbar and limb muscles. SBMA is caused by a CAG repeat expansion in the gene that encodes the androgen receptor (AR) protein. Disease manifestation is androgen dependent and results principally from a toxic gain of AR function. There are currently no effective treatments for this debilitating disease. It is important to understand the course of the disease in order to target therapeutics to key pathological stages. This is especially relevant in disorders such as SBMA, where disease can be identified prior to symptom onset, through family history and genetic testing. To fully characterise the role of muscle in SBMA, we undertook a longitudinal physiological and histological characterisation of disease progression in the AR100 mouse model of SBMA. Our results show that the disease first manifests in skeletal muscle, prior to any motor neuron degeneration, which only occurs in late stage disease. These findings reveal alterations in muscle function, including reduced muscle force and changes in contractile characteristics, are early pathological events in SBMA mice and suggest that muscle-targeted therapeutics may be effective in SBMA.<\/jats:p>","DOI":"10.1242\/dmm.042424","type":"journal-article","created":{"date-parts":[[2020,3,9]],"date-time":"2020-03-09T23:15:14Z","timestamp":1583795714000},"source":"Crossref","is-referenced-by-count":10,"title":["Deterioration of muscle force and contractile characteristics are early pathological events in spinal and bulbar muscular atrophy mice"],"prefix":"10.1242","author":[{"given":"Anna L.","family":"Gray","sequence":"first","affiliation":[{"name":"Department of Neuromuscular Diseases, UCL Queen Square Institute of Neurology, Queen Square, London WC1N 3BG, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Leonette","family":"Annan","sequence":"additional","affiliation":[{"name":"Department of Neuromuscular Diseases, UCL Queen Square Institute of Neurology, Queen Square, London WC1N 3BG, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"James R. T.","family":"Dick","sequence":"additional","affiliation":[{"name":"Department of Neuromuscular Diseases, UCL Queen Square Institute of Neurology, Queen Square, London WC1N 3BG, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Albert R.","family":"La Spada","sequence":"additional","affiliation":[{"name":"Departments of Neurology, Duke University School of Medicine, Durham, USA"},{"name":"Neurobiology, Duke University School of Medicine, Durham, USA"},{"name":"Cell Biology, Duke University School of Medicine, Durham, USA"},{"name":"Duke Centre for Neurodegeneration & Neurotherapeutics, Duke University School of Medicine, Durham, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael G.","family":"Hanna","sequence":"additional","affiliation":[{"name":"Department of Neuromuscular Diseases, UCL Queen Square Institute of Neurology, Queen Square, London WC1N 3BG, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Linda","family":"Greensmith","sequence":"additional","affiliation":[{"name":"Department of Neuromuscular Diseases, UCL Queen Square Institute of Neurology, Queen Square, London WC1N 3BG, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3527-0102","authenticated-orcid":false,"given":"Bilal","family":"Malik","sequence":"additional","affiliation":[{"name":"Department of Neuromuscular Diseases, UCL Queen Square Institute of Neurology, Queen Square, London WC1N 3BG, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"237","published-online":{"date-parts":[[2020,1,1]]},"reference":[{"key":"2021042700234825600_DMM042424C1","doi-asserted-by":"publisher","first-page":"659","DOI":"10.1093\/brain\/awh381","article-title":"Widespread nuclear and cytoplasmic accumulation of mutant androgen receptor in SBMA patients","volume":"128","author":"Adachi","year":"2005","journal-title":"Brain"},{"key":"2021042700234825600_DMM042424C2","doi-asserted-by":"publisher","first-page":"1199","DOI":"10.1021\/acs.biochem.6b00936","article-title":"Proteins containing expanded polyglutamine tracts and neurodegenerative disease","volume":"56","author":"Adegbuyiro","year":"2017","journal-title":"Biochemistry"},{"key":"2021042700234825600_DMM042424C3","doi-asserted-by":"publisher","first-page":"1446","DOI":"10.1093\/brain\/awl096","article-title":"Natural history of spinal and bulbar muscular atrophy (SBMA): a study of 223 Japanese patients","volume":"129","author":"Atsuta","year":"2006","journal-title":"Brain"},{"key":"2021042700234825600_DMM042424C4","doi-asserted-by":"publisher","first-page":"427","DOI":"10.1038\/nm.4500","article-title":"Selective modulation of the androgen receptor AF2 domain rescues degeneration in spinal bulbar muscular atrophy","volume":"24","author":"Badders","year":"2018","journal-title":"Nat. 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