ArticleBrain pathology (Zurich, Switzerland)2023
Cerebellar structural, astrocytic, and neuronal abnormalities in the SMNΔ7 mouse model of spinal muscular atrophy.
Article in Brain pathology (Zurich, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Protocol for diffusion magnetic resonance imaging and tractography in ex vivo mouse models.STAR protocols · 2026Article
- Cerebellar pathology contributes to neurodevelopmental deficits in spinal muscular atrophy.Brain : a journal of neurology · 2026Article
- Survival motor neuron protein-independent amelioration of spinal muscular atrophy by pharmacological inhibition of c-Jun-NHBrain communications · 2026Article
- Cerebellar defects are a primary pathology in mouse models of spinal muscular atrophy.Brain pathology (Zurich, Switzerland) · 2025Article
- From Circuits to Lifespan: Translating Mouse and Human Timelines with Neuroimaging-Based Tractography.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Quantitative synthetic MRI reveals grey matter abnormalities in patients with spinal muscular atrophy types 2 and 3.Quantitative imaging in medicine and surgery · 2025Article
- From circuits to lifespan: translating mouse and human timelines with neuroimaging based tractography.bioRxiv : the preprint server for biology · 2024Article
- Disrupted individual-level morphological brain network in spinal muscular atrophy types 2 and 3.CNS neuroscience & therapeutics · 2024Article
- No significant sex differences in incidence or phenotype for the SMNΔ7 mouse model of spinal muscular atrophy.Neuromuscular disorders : NMD · 2024Article
- Cerebellar structural, astrocytic, and neuronal abnormalities in the SMNΔ7 mouse model of spinal muscular atrophy.Brain pathology (Zurich, Switzerland) · 2023Article
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7 authors.
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Abstract
Spinalmuscular atrophy (SMA) is a neuromuscular disease that affects as many as 1 in 6000 individuals at birth, making it the leading genetic cause of infant mortality. A growing number of studies indicate that SMA is a multi-system disease. The cerebellum has received little attention even though it plays an important role in motor function and widespread pathology has been reported in the cerebella of SMA patients. In this study, we assessed SMA pathology in the cerebellum using structural and diffusion magnetic resonance imaging, immunohistochemistry, and electrophysiology with the SMNΔ7 mouse model. We found a significant disproportionate loss in cerebellar volume, decrease in afferent cerebellar tracts, selective lobule-specific degeneration of Purkinje cells, abnormal lobule foliation and astrocyte integrity, and a decrease in spontaneous firing of cerebellar output neurons in the SMA mice compared to controls. Our data suggest that defects in cerebellar structure and function due to decreased survival motor neuron (SMN) levels impair the functional cerebellar output affecting motor control, and that cerebellar pathology should be addressed to achieve comprehensive treatment and therapy for SMA patients.
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