ArticleFrontiers in molecular neuroscience2020
Brain Dysfunction in LAMA2-Related Congenital Muscular Dystrophy: Lessons From Human Case Reports and Mouse Models.
Article in Frontiers in molecular neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed, 42 citations in OpenAlex.
- A Role for Astrocyte Metabolism in Species-Specific Neuronal Development.bioRxiv : the preprint server for biology · 2026Article
- Roles and therapeutic prospects of the laminin family in disorders of the nervous system.Journal of translational medicine · 2026Review
- A novel mouse model foreLife · 2025Article
- The landscape of pediatric genetic white matter disorders at a tertiary referral hospital in Upper Egypt and the report of 31 novel variants.Italian journal of pediatrics · 2025Article
- RNA-binding proteins potentially regulate the alternative splicing of apoptotic genes during knee osteoarthritis progression.BMC genomics · 2024Article
- Pharmacotherapeutic Approaches to Treatment of Muscular Dystrophies.Biomolecules · 2023Review
- Extension of the Clinicoradiologic Spectrum of Newly Described End-TruncatingNeurology. Genetics · 2023Article
- The alpha7 integrin subunit in astrocytes promotes endothelial blood-brain barrier integrity.Development (Cambridge, England) · 2023Article
- Unique genotype-phenotype correlations withinFrontiers in neurology · 2023Article
- Observational
- Brain MRI Abnormalities, Epilepsy and Intellectual Disability in LAMA2 Related Dystrophy - a Genotype/Phenotype Correlation.Journal of neuromuscular diseases · 2023Observational
- LAMA2-related muscular dystrophy mimicking multiple sclerosis.BMJ case reports · 2022Article
- The molecular regulation of oligodendrocyte development and CNS myelination by ECM proteins.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Laminin α2 gene (LAMA2)-related Congenital Muscular Dystrophy (CMD) was distinguished by a defining central nervous system (CNS) abnormality-aberrant white matter signals by MRI-when first described in the 1990s. In the past 25 years, researchers and clinicians have expanded our knowledge of brain involvement in LAMA2-related CMD, also known as Congenital Muscular Dystrophy Type 1A (MDC1A). Neurological changes in MDC1A can be structural, including lissencephaly and agyria, as well as functional, including epilepsy and intellectual disability. Mouse models of MDC1A include both spontaneous and targeted LAMA2 mutations and range from a partial loss of LAMA2 function (e.g.,
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Registered trials
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