ReviewCNS neuroscience & therapeutics2025
Neuronal Ceroid Lipofuscinosis-Concepts, Classification, and Avenues for Therapy.
Review in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- The role of protein palmitoylation in disease pathogenesis and therapeutic innovation.Annals of medicine · 2026Review
- Astrocytes in Neurodegeneration: Spatial States, Crosstalk, and Emerging Therapies.Molecular neurobiology · 2026Review
- Neurodegenerative Diseases in Children: A Comprehensive Review.International journal of molecular sciences · 2026Review
- A Flupirtine Benzyl Carbamate Improves Neurocognitive Deficits and Molecular Pathology in theCells · 2026Article
- Prosaposin Is Cleaved Into Saposins by Multiple Cathepsins in a Progranulin-Regulated Fashion.Journal of neurochemistry · 2026Article
- The Clinical Burden of Inherited Neurometabolic Disorders in Adults-A Territorial Care Approach.Journal of clinical medicine · 2025Article
- Prodromal pathogenesis of CLN7 Batten Disease revealed by multimodal biomarkers in macaques.bioRxiv : the preprint server for biology · 2025Article
- Canine Neuronal Ceroid Lipofuscinosis-like Disorder Associated with Sequence Variants inGenes · 2025Article
- The first report of ceroid lipofuscinosis type 11 in China: a novel mutation of GRN and updated clinical review.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Review
- Is the Voltage-Dependent Anion Channel a Major Player in Neurodegenerative Diseases?International journal of molecular sciences · 2025Review
- Diagnostic analysis of adult neuronal ceroid lipofuscinosis caused by CLN6 gene mutation: a case report.Clinical parkinsonism & related disorders · 2025Article
- Case Report: The window that closed too soon: lessons from a late CLN2 diagnosis and death of a 9-year-old boy.Frontiers in genetics · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Neuronal ceroid lipofuscinosis (NCL) is a group of neurodegenerative lysosomal storage disorders characterized by excessive accumulation of lysosomal lipofuscin. Thirteen subtypes of NCL have been identified, each associated with distinct genes encoding various transmembrane proteins, secretory proteins, or lysosomal enzymes. Clinically, NCL manifests in infants through vision impairment, motor and cognitive dysfunctions, epilepsy, and premature death. The pathological complexity of NCL has hindered the development of effective clinical protocols. Current treatment modalities, including enzyme replacement therapy, pharmacological approaches, gene therapy, and stem cell therapy, have demonstrated limited efficacy. However, emerging evidence suggests a significant relationship between NCL and microglial cells, highlighting the potential of novel microglial cell replacement therapies. This review comprehensively examines the pathogenic genes associated with various NCL subtypes, elucidating their roles, clinical presentations, and corresponding mouse models. Especially, we thoroughly discuss the advances in the clinical study of potential therapeutics, which crucially calls for early diagnosis and treatment more than ever.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.