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Mechanisms of Skeletal Muscle Adaptation to Resistance Training in Spinal Muscular Atrophy

Project description

Strength exercise therapy for spinal muscular atrophy

Spinal muscular atrophy (SMA) is a rare genetic disorder associated with progressive loss of motor neurons, leading to muscle weakness and atrophy. It is caused by a deficiency of the survival motor neuron (SMN) protein, which is essential for motor neuron function and muscle maintenance. Although SMN-targeting therapies are beneficial, additional strategies are needed to support long-term health and improve quality of life. With the support of the Marie Skłodowska-Curie Actions programme, the SMA-RT project will investigate the impact of resistance training in SMA. Researchers will employ transgenic mouse models to study the morphological, functional, and molecular responses to exercise. The goal is to conduct a clinical trial in SMA patients and establish physical training as supportive therapy.

Objective

Spinal Muscular Atrophy (SMA) is a debilitating neuromuscular disorder characterised by progressive motoneuron degeneration, which causes muscle atrophy and weakness. By combining pre-clinical studies and a clinical trial, this 36-month Global Fellowship aims to explore the beneficial role of exercise as a therapeutic strategy to support SMA treatment and improve clinical outcomes. During my outgoing phase at Harvard University, I will employ two transgenic SMA mouse models to investigate the skeletal muscle adaptations to overloading, achieved via synergistic ablation, a model historically used to study muscle hypertrophy and mimic human resistance training. In WP1, I will investigate the muscle morphological, functional, and transcriptomic responses to overloading in SMNΔ7 mutant mice, which, similarly to patients, present ubiquitous SMN deficiency and lifespan extension via pharmacological treatment. In WP2, I will perform the same overloading protocol and similar analyses on a mouse model presenting SMN knockout restricted to muscle satellite cells (Pax7:SMN-KO). While ubiquitous SMN deficiency triggers motoneuron degeneration, this model enables to focus on the role of satellite cells in SMA by deleting SMN selectively in these cells. During my incoming phase at the University of Padova, I will assess whether the molecular mechanisms underlying muscle adaptation identified in mice are translatable to humans, examining the response of SMA type III/IV patients, presenting the milder form of SMA, to a resistance training intervention (WP3). I will employ musculoskeletal imaging techniques, advanced EMG methods, and muscle biopsy and blood sample analysis to perform a comprehensive analysis, which is lacking to date. This project aims to propose exercise as a novel strategy to improve the quality of life in patients affected by SMA and other devastating neuromuscular disorders, also reducing the heavy socioeconomic burden associated with these diseases.

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HORIZON-TMA-MSCA-PF-GF - HORIZON TMA MSCA Postdoctoral Fellowships - Global Fellowships

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Call for proposal

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(opens in new window) HORIZON-MSCA-2024-PF-01

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Coordinator

UNIVERSITA DEGLI STUDI DI PADOVA
Net EU contribution

Net EU financial contribution. The sum of money that the participant receives, deducted by the EU contribution to its linked third party. It considers the distribution of the EU financial contribution between direct beneficiaries of the project and other types of participants, like third-party participants.

€ 396 991,08
Address
VIA 8 FEBBRAIO 2
35122 PADOVA
Italy

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Region
Nord-Est Veneto Padova
Activity type
Higher or Secondary Education Establishments
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Total cost

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