ArticleNeurobiology of aging2010
Amyloid-β protein impairs Ca2+ release and contractility in skeletal muscle.
Article in Neurobiology of aging, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 59 citations in OpenAlex.
- Molecular Mechanisms and Therapeutic Potential of DJ-1 in Skeletal Muscle Homeostasis and Disease.Comprehensive Physiology · 2026Review
- Trajectories of physical functioning and its implication for all-cause mortality in Chinese older people: a large-scale national longitudinal study.Journal of global health · 2025Article
- Effects and mechanisms of APP and its cleavage product Aβ in the comorbidity of sarcopenia and Alzheimer's disease.Frontiers in aging neuroscience · 2024Review
- APP in the Neuromuscular Junction for the Development of Sarcopenia and Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Review
- Elevating the Levels of Calcium Ions Exacerbate Alzheimer's Disease via Inducing the Production and Aggregation of β-Amyloid Protein and Phosphorylated Tau.International journal of molecular sciences · 2021Review
- The Relevance of Amyloid β-Calmodulin Complexation in Neurons and Brain Degeneration in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Programmed Cell Death Pathways in the Pathogenesis of Idiopathic Inflammatory Myopathies.Frontiers in immunology · 2021Review
- Can the Energetic Profile of Skeletal Muscle Predict Risk of Cognitive Impairment?Function (Oxford, England) · 2021Article
- Alterations of the Endoplasmic Reticulum (ER) Calcium Signaling Molecular Components in Alzheimer's Disease.Cells · 2020Review
- Cell Death and Neurodegeneration.Cold Spring Harbor perspectives in biology · 2020Review
- Hyperactivity Induced by Soluble Amyloid-β Oligomers in the Early Stages of Alzheimer's Disease.Frontiers in molecular neuroscience · 2020Review
- Desmin forms toxic, seeding-competent amyloid aggregates that persist in muscle fibers.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Physical Frailty and Amyloid-β Deposits in the Brains of Older Adults with Cognitive Frailty.Journal of clinical medicine · 2018Article
- Multiple mechanisms of dimethyl fumarate in amyloid β-induced neurotoxicity in human neuronal cells.Journal of cellular and molecular medicine · 2018Article
- Article
- The Immune Response and the Pathogenesis of Idiopathic Inflammatory Myositis: a Critical Review.Clinical reviews in allergy & immunology · 2017Review
- Increased amyloid β-peptide uptake in skeletal muscle is induced by hyposialylation and may account for apoptosis in GNE myopathy.Oncotarget · 2016Article
- Amyloid beta peptide 22-35 induces a negative inotropic effect on isolated rat hearts.International journal of physiology, pathophysiology and pharmacology · 2016Article
- Phosphoinositides in Ca(2+) signaling and excitation-contraction coupling in skeletal muscle: an old player and newcomers.Journal of muscle research and cell motility · 2015Review
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 3 countries.
Funding
Abstract
Inclusion body myositis (IBM), the most common muscle disorder in the elderly, is partly characterized by dysregulation of β-amyloid precursor protein (βAPP) expression and abnormal, intracellular accumulation of full-length βAPP and β-amyloid epitopes. The present study examined the effects of β-amyloid accumulation on force generation and Ca(2+) release in skeletal muscle from transgenic mice harboring human βAPP and assessed the consequence of Aβ(1-42) modulation of the ryanodine receptor Ca(2+) release channels (RyRs). β-Amyloid laden muscle produced less peak force and exhibited Ca(2+) transients with smaller amplitude. To determine whether modification of RyRs by β-amyloid underlie the effects observed in muscle, in vitro Ca(2+) release assays and RyR reconstituted in planar lipid bilayer experiments were conducted in the presence of Aβ(1-42). Application of Aβ(1-42) to RyRs in bilayers resulted in an increased channel open probability and changes in gating kinetics, while addition of Aβ(1-42) to the rabbit SR vesicles resulted in RyR-mediated Ca(2+) release. These data may relate altered βAPP metabolism in IBM to reductions in RyR-mediated Ca(2+) release and muscle contractility.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.