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 β (APPβ) and APP in the prefrontal cortex of
mdx
mice compared with WT, and lower soluble APPα 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.