ArticlePloS one2018
Defects in nerve conduction velocity and different muscle fibre-type specificity contribute to muscle weakness in Ts1Cje Down syndrome mouse model.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Meta-analysis of metabolites involved in bioenergetic pathways reveals a pseudohypoxic state in Down syndrome.Molecular medicine (Cambridge, Mass.) · 2020Pooled it
- Habitual lip and tongue posture in infants with Trisomy 21: characterization and associated factors.CoDAS · 2026Observational
- Virtual Reality-Based Therapy Can Enhance Balance and Muscular Endurance in Children and Adolescents with Down Syndrome: A Systematic Review with a Meta-Analysis.Bioengineering (Basel, Switzerland) · 2024Review
- Bruxism in a Child with Trisomy 21 (Down Syndrome)-Case Report.Journal of clinical medicine · 2024Article
- Body composition parameters and sarcopenia in adults with Down syndrome: a case-control study.Aging clinical and experimental research · 2024Article
- Electromyographic Study of Masticatory Muscle Function in Children with Down Syndrome.Journal of clinical medicine · 2022Article
- Trans-synaptic spreading of alpha-synuclein pathology through sensory afferents leads to sensory nerve degeneration and neuropathic pain.Acta neuropathologica communications · 2021Article
- Addressing the Need of a Translational Approach in Peripheral Neuropathy Research: Morphology Meets Function.Brain sciences · 2021Article
- Phenotype microarrays reveal metabolic dysregulations of neurospheres derived from embryonic Ts1Cje mouse model of Down syndrome.PloS one · 2020Article
- Peripheral Nerve Regeneration Is Independent From Schwann Cell p75Frontiers in cellular neuroscience · 2019Article
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDown syndrome (DS) is a genetic disorder caused by presence of extra copy of human chromosome 21. It is characterised by several clinical phenotypes. Motor dysfunction due to hypotonia is commonly seen in individuals with DS and its etiology is yet unknown. Ts1Cje, which has a partial trisomy (Mmu16) homologous to Hsa21, is well reported to exhibit various typical neuropathological features seen in individuals with DS. This study investigated the role of skeletal muscles and peripheral nerve defects in contributing to muscle weakness in Ts1Cje mice.
resultsAssessment of the motor performance showed that, the forelimb grip strength was significantly (P<0.0001) greater in the WT mice compared to Ts1Cje mice regardless of gender. The average survival time of the WT mice during the hanging wire test was significantly (P<0.0001) greater compared to the Ts1Cje mice. Also, the WT mice performed significantly (P<0.05) better than the Ts1Cje mice in the latency to maintain a coordinated motor movement against the rotating rod. Adult Ts1Cje mice exhibited significantly (P<0.001) lower nerve conduction velocity compared with their aged matched WT mice. Further analysis showed a significantly (P<0.001) higher population of type I fibres in WT compared to Ts1Cje mice. Also, there was significantly (P<0.01) higher population of COX deficient fibres in Ts1Cje mice. Expression of Myf5 was significantly (P<0.05) reduced in triceps of Ts1Cje mice while MyoD expression was significantly (P<0.05) increased in quadriceps of Ts1Cje mice.
conclusionTs1Cje mice exhibited weaker muscle strength. The lower population of the type I fibres and higher population of COX deficient fibres in Ts1Cje mice may contribute to the muscle weakness seen in this mouse model for DS.
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