ArticleMolecular neurobiology2022
Lack of p62 Impairs Glycogen Aggregation and Exacerbates Pathology in a Mouse Model of Myoclonic Epilepsy of Lafora.
Article in Molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- An astrocytic cellular model of Lafora disease to study polyglucosan accumulation and inflammation.Disease models & mechanisms · 2026Article
- Brain Glycogen-Its Metabolic Role in Neuronal Health and Neurological Disorders-An Extensive Narrative Review.Metabolites · 2025Review
- Autophagy-related genes in mesial temporal lobe epilepsy: an integrated bioinformatics analysis.Acta epileptologica · 2024Article
- Role of Astrocytes in the Pathophysiology of Lafora Disease and Other Glycogen Storage Disorders.Cells · 2023Review
- Glial Contributions to Lafora Disease: A Systematic Review.Biomedicines · 2022Review
- Autophagy Modulation in Aggresome Formation: Emerging Implications and Treatments of Alzheimer's Disease.Biomedicines · 2022Review
- Malin restoration as proof of concept for gene therapy for Lafora disease.Brain communications · 2022Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Lafora disease (LD) is a fatal childhood-onset dementia characterized by the extensive accumulation of glycogen aggregates-the so-called Lafora Bodies (LBs)-in several organs. The accumulation of LBs in the brain underlies the neurological phenotype of the disease. LBs are composed of abnormal glycogen and various associated proteins, including p62, an autophagy adaptor that participates in the aggregation and clearance of misfolded proteins. To study the role of p62 in the formation of LBs and its participation in the pathology of LD, we generated a mouse model of the disease (malin
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Registered trials
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