Mitochondrial oxygen consumption deficits in skeletal muscle isolated from an Alzheimer’s disease-relevant murine model

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dc.contributor.authorSchuh, Rosemary A
dc.contributor.authorJackson, Kathryn C
dc.contributor.authorSchlappal, Anna E
dc.contributor.authorSpangenburg, Espen E
dc.contributor.authorWard, Christopher W
dc.contributor.authorPark, Ji H
dc.contributor.authorDugger, Natalie
dc.contributor.authorShi, Guo Li
dc.contributor.authorFishman, Paul S
dc.date.accessioned2021-09-21T17:03:57Z
dc.date.available2021-09-21T17:03:57Z
dc.date.issued2014-02-13
dc.description.abstractAge is considered a primary risk factor for neurodegenerative diseases including Alzheimer’s disease (AD). It is also now well understood that mitochondrial function declines with age. Mitochondrial deficits have been previously assessed in brain from both human autopsy tissue and disease-relevant transgenic mice. Recently it has been recognized that abnormalities of muscle may be an intrinsic aspect of AD and might contribute to the pathophysiology. However, deficits in mitochondrial function have yet to be clearly assessed in tissues outside the central nervous system (CNS). In the present study, we utilized a well-characterized AD-relevant transgenic mouse strain to assess mitochondrial respiratory deficits in both brain and muscle. In addition to mitochondrial function, we assessed levels of transgene-derived amyloid precursor protein (APP) in homogenates isolated from brain and muscle of these AD-relevant animals. We now demonstrate that skeletal muscles isolated from these animals have differential levels of mutant full-length APP depending on muscle type. Additionally, isolated muscle fibers from young transgenic mice (3 months) have significantly decreased maximal mitochondrial oxygen consumption capacity compared to non-transgenic, age-matched mice, with similar deficits to those previously described in brain. This is the first study to directly examine mitochondrial function in skeletal muscle from an AD-relevant transgenic murine model. As with brain, these deficits in muscle are an early event, occurring prior to appearance of amyloid plaques.en_US
dc.description.urihttps://doi.org/10.1186/1471-2202-15-24
dc.identifierhttps://doi.org/10.13016/pq5t-ictg
dc.identifier.citationSchuh, R.A., Jackson, K.C., Schlappal, A.E. et al. Mitochondrial oxygen consumption deficits in skeletal muscle isolated from an Alzheimer’s disease-relevant murine model. BMC Neurosci 15, 24 (2014).en_US
dc.identifier.urihttp://hdl.handle.net/1903/27898
dc.language.isoen_USen_US
dc.publisherSpringer Natureen_US
dc.relation.isAvailableAtSchool of Public Healthen_us
dc.relation.isAvailableAtKinesiologyen_us
dc.relation.isAvailableAtDigital Repository at the University of Marylanden_us
dc.relation.isAvailableAtUniversity of Maryland (College Park, MD)en_us
dc.subjectAlzheimer’s diseaseen_US
dc.subjectMitochondriaen_US
dc.subjectAmyloid plaqueen_US
dc.subjectNeurodegenerationen_US
dc.subjectMuscleen_US
dc.titleMitochondrial oxygen consumption deficits in skeletal muscle isolated from an Alzheimer’s disease-relevant murine modelen_US
dc.typeArticleen_US

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