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    Characterization of Alzheimer's disease‐like neuropathology in Duchenne's muscular dystrophy using the DBA/2J mdx mouse model

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    Author
    Hayward, Grant C.
    Caceres, Daniela
    Copeland, Emily N.
    Baranowski, Bradley J.
    Mohammad, Ahmad
    Whitley, Kennedy C.
    Fajardo, Val A.
    MacPherson, Rebecca E. K.
    Keyword
    Alzheimer’s disease
    amyloid
    brain
    cognition
    Duchenne muscular dystrophy
    muscular dystrophy
    Journal title
    FEBS Open Bio
    Publication Volume
    12
    Publication Issue
    1
    Publication Begin page
    154
    Publication End page
    162
    
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    URI
    http://hdl.handle.net/10464/15629
    Abstract
    Duchenne muscular dystrophy (DMD) is a progressive muscle wasting disorder caused by a mutation in the dystrophin gene. In addition to muscle pathology, some patients with DMD will exhibit cognitive impairments with severity being linked to age and type of genetic mutation. Likewise, some studies have shown that mdx mice display impairments in spatial memory compared with wild-type (WT) controls, while others have not observed any such effect. Most studies have utilized the traditional C57BL/10 (C57) mdx mouse, which exhibits a mild disease phenotype. Recently, the DBA/2J (D2) mdx mouse has emerged as a more severe and perhaps clinically relevant DMD model; however, studies examining cognitive function in these mice are limited. Thus, in this study we examined cognitive function in age-matched C57 and D2 mdx mice along with their respective WT controls. Our findings show that 8- to 12-week-old C57 mdx mice did not display any differences in exploration time when challenged with a novel object recognition test. Conversely, age-matched D2 mdx mice spent less time exploring objects in total as a well as less time exploring the novel object, suggestive of impaired recognition memory. Biochemical analyses of the D2 mdx brain revealed higher soluble amyloid precursor protein b(APPb) and APP in the prefrontal cortex of mdx mice compared with WT, and lower soluble APPa in the hippocampus, suggestive of a shift towards amyloidogenesis and a similar pathogenesis to Alzheimer’s disease. Furthermore, our study demonstrates the utility of the D2 mdx model in studying cognitive impairment.
    ae974a485f413a2113503eed53cd6c53
    10.1002/2211-5463.13317
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    2021 Open Access Fund Recipients

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