ArticleAging cell2014
Neuronal glycogen synthesis contributes to physiological aging.
Article in Aging cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 88 citations in OpenAlex.
- Corpora amylacea profiling reveals disease stage and brain region-specific alterations in glycogen metabolism in Alzheimer's disease patient brains.Cell reports. Medicine · 2026Article
- PYGL-driven glycogenolysis impairs microglial autophagic fluxActa pharmaceutica Sinica. B · 2026Article
- Glycogen drives the sensory activation of POMC neurons.Nature metabolism · 2026Article
- Inactivation of Laforin Phosphatase and Increased Glucose Uptake Underlie Glycogen Synthase-Mediated Neuronal Survival Under Oxidative Stress.Molecular neurobiology · 2025Article
- Hepatic glycogen directly regulates gluconeogenesis through an AMPK/CRTC2 axis in mice.The Journal of clinical investigation · 2025Article
- A Bird's-Eye View of Glycolytic Upregulation in Activated Brain: The Major Fate of Lactate Is Release From Activated Tissue, Not Shuttling to Nearby Neurons.Journal of neurochemistry · 2025Review
- Glycogen synthase is required for heat shock-mediated autophagy induction in neuronal cells.Biology open · 2025Article
- Dapagliflozin ameliorates Lafora disease phenotype in a zebrafish model.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Article
- Preventing excessive autophagy protects from the pathology of mtDNA mutations in Drosophila melanogaster.Nature communications · 2024Article
- Gene therapy for Lafora disease in the Epm2aMolecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Glycogen accumulation modulates life span in a mouse model of amyotrophic lateral sclerosis.Journal of neurochemistry · 2024Article
- Increase in brain glycogen levels ameliorates Huntington's disease phenotype and rescues neurodegeneration in Drosophila.Disease models & mechanisms · 2023Article
- Glutamine metabolism in diseases associated with mitochondrial dysfunction.Molecular and cellular neurosciences · 2023Review
- 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
- Corpora amylacea are associated with tau burden and cognitive status in Alzheimer's disease.Acta neuropathologica communications · 2022Article
- Trehalose Treatment in Zebrafish Model of Lafora Disease.International journal of molecular sciences · 2022Article
- Lafora disease: Current biology and therapeutic approaches.Revue neurologique · 2022Review
- Deconvolution of the epigenetic age discloses distinct inter-personal variability in epigenetic aging patterns.Epigenetics & chromatin · 2022Article
- Lack of p62 Impairs Glycogen Aggregation and Exacerbates Pathology in a Mouse Model of Myoclonic Epilepsy of Lafora.Molecular neurobiology · 2022Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glycogen is a branched polymer of glucose and the carbohydrate energy store for animal cells. In the brain, it is essentially found in glial cells, although it is also present in minute amounts in neurons. In humans, loss-of-function mutations in laforin and malin, proteins involved in suppressing glycogen synthesis, induce the presence of high numbers of insoluble polyglucosan bodies in neuronal cells. Known as Lafora bodies (LBs), these deposits result in the aggressive neurodegeneration seen in Lafora's disease. Polysaccharide-based aggregates, called corpora amylacea (CA), are also present in the neurons of aged human brains. Despite the similarity of CA to LBs, the mechanisms and functional consequences of CA formation are yet unknown. Here, we show that wild-type laboratory mice also accumulate glycogen-based aggregates in the brain as they age. These structures are immunopositive for an array of metabolic and stress-response proteins, some of which were previously shown to aggregate in correlation with age in the human brain and are also present in LBs. Remarkably, these structures and their associated protein aggregates are not present in the aged mouse brain upon genetic ablation of glycogen synthase. Similar genetic intervention in Drosophila prevents the accumulation of glycogen clusters in the neuronal processes of aged flies. Most interestingly, targeted reduction of Drosophila glycogen synthase in neurons improves neurological function with age and extends lifespan. These results demonstrate that neuronal glycogen accumulation contributes to physiological aging and may therefore constitute a key factor regulating age-related neurological decline in humans.
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