ArticleFrontiers in aging neuroscience2022
Age Related Changes in Muscle Mass and Force Generation in the Triple Transgenic (3xTgAD) Mouse Model of Alzheimer's Disease.
Article in Frontiers in aging neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 21 citations in OpenAlex.
- Evaluating the peripheral nervous system pathology of Alzheimer's disease utilizing a functional human NMJ microphysiological system.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Integrative physiology of skeletal muscle for maintaining cognitive health.The Journal of physiology · 2026Review
- Soft tissue changes in Dementia: A comprehensive systematic review.Aging brain · 2026Review
- Physical exercise mitigates motor and muscular deficits in the 3xTg-AD model of Alzheimer's disease.Frontiers in aging neuroscience · 2026Article
- Neural Cues and Genomic Clues: NGS Insights into Neurogenic Sarcopenia and Muscle Atrophy.International journal of molecular sciences · 2025Review
- CORP: In vivo muscle strength-perspectives on the design and interpretation of preclinical animal studies.American journal of physiology. Regulatory, integrative and comparative physiology · 2025Review
- Research progress on resistance exercise therapy for improving cognitive function in patients with AD and muscle atrophy.Frontiers in aging neuroscience · 2025Review
- Alzheimer's Disease: Understanding Motor Impairments.Brain sciences · 2024Review
- Neuroprotective treatment with the nitrone compound OKN-007 mitigates age-related muscle weakness in aging mice.GeroScience · 2024Article
- Review
- Sarcopenia is a predictor for Alzheimer's continuum and related clinical outcomes.Scientific reports · 2024Article
- Cognition as mediator of pulmonary function and risk of sarcopenia among older adults.BMC public health · 2024Article
- Targeted brain-specific tauopathy compromises peripheral skeletal muscle integrity and function.Aging brain · 2024Article
- Effects and mechanisms of APP and its cleavage product Aβ in the comorbidity of sarcopenia and Alzheimer's disease.Frontiers in aging neuroscience · 2024Review
- Neuromuscular Dysfunction Precedes Cognitive Impairment in a Mouse Model of Alzheimer's Disease.Function (Oxford, England) · 2024Article
- The nitrone compound OKN-007 delays motor neuron loss and disease progression in the G93A mouse model of amyotrophic lateral sclerosis.Frontiers in neuroscience · 2024Article
- Targeted brain-specific tauopathy compromises peripheral skeletal muscle integrity and function.bioRxiv : the preprint server for biology · 2023Article
- APP in the Neuromuscular Junction for the Development of Sarcopenia and Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Development of a system to analyze oral frailty associated with Alzheimer's disease using a mouse model.Frontiers in aging neuroscience · 2022Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Emerging evidence suggests that patients with Alzheimer's disease (AD) may show accelerated sarcopenia phenotypes. To investigate whether pathological changes associated with neuronal death and cognitive dysfunction also occur in peripheral motor neurons and muscle as a function of age, we used the triple transgenic mouse model of AD (3xTgAD mice) that carries transgenes for mutant forms of APP, Tau, and presenilin proteins that are associated with AD pathology. We measured changes in motor neurons and skeletal muscle function and metabolism in young (2 to 4 month) female control and 3xTgAD mice and in older (18-20 month) control and 3xTgAD female mice. In older 3xTgAD mice, we observed a number of sarcopenia-related phenotypes, including significantly fragmented and denervated neuromuscular junctions (NMJs) associated with a 17% reduction in sciatic nerve induced vs. direct muscle stimulation induced contractile force production, and a 30% decrease in gastrocnemius muscle mass. On the contrary, none of these outcomes were found in young 3xTgAD mice. We also measured an accumulation of amyloid-β (Aβ) in both skeletal muscle and neuronal tissue in old 3xTgAD mice that may potentially contribute to muscle atrophy and NMJ disruption in the older 3xTgAD mice. Furthermore, the TGF-β mediated atrophy signaling pathway is activated in old 3xTgAD mice and is a potential contributing factor in the muscle atrophy that occurs in this group. Perhaps surprisingly, mitochondrial oxygen consumption and reactive oxygen species (ROS) production are not elevated in skeletal muscle from old 3xTgAD mice. Together, these results provide new insights into the effect of AD pathological mechanisms on peripheral changes in skeletal muscle.
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