ArticleEpilepsia2022
Increased expression of complement components in tuberous sclerosis complex and focal cortical dysplasia type 2B brain lesions.
Article in Epilepsia, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Molecular Signature in Focal Cortical Dysplasia: A Systematic Review of RNA and Protein Data.International journal of molecular sciences · 2025Pooled it
- The Mechanism Underlying the Abnormal Expression of α-Synuclein in the Cortical Lesions of Patients With FCD Type IIb and TSC.CNS neuroscience & therapeutics · 2026Article
- Microglial phagocytosis in epilepsy: Mechanisms and impact.The Journal of physiology · 2026Review
- Temporal lobe epilepsy is associated with neuroinflammation, extracellular matrix remodeling, and synaptic protein alterations.Frontiers in molecular neuroscience · 2026Article
- Microglial pathological synaptic pruning in epilepsy: pathophysiology and therapeutic potential.Frontiers in immunology · 2026Review
- Beyond mTOR: Unraveling the Complex Pathophysiology and Signaling Pathways in Focal Cortical Dysplasia.Molecular neurobiology · 2025Review
- Organophosphate Chemical Nerve Agents, Oxidative Stress, and NADPH Oxidase Inhibitors: An Overview.International journal of molecular sciences · 2025Review
- The Activation of the Microglial NLRP3 Inflammasome Is Involved in Tuberous Sclerosis Complex-Related Neuroinflammation.International journal of molecular sciences · 2025Article
- WONOEP appraisal: The role of glial cells in focal malformations associated with early onset epilepsies.Epilepsia · 2024Review
- CNS autoimmune response in the MAM/pilocarpine rat model of epileptogenic cortical malformation.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Is tuberous sclerosis complex-associated autism a preventable and treatable disorder?World journal of pediatrics : WJP · 2024Review
- Article
- Epileptogenesis in tuberous sclerosis complex-related developmental and epileptic encephalopathy.Brain : a journal of neurology · 2023Review
- Astrocyte-derived complement C3 is activated in patients with tuberous sclerosis complex and mediates immune injury: an integrated bioinformatics analysis.Translational pediatrics · 2023Article
- Dendritic spine loss in epileptogenic Type II focal cortical dysplasia: Role of enhanced classical complement pathway activation.Brain pathology (Zurich, Switzerland) · 2023Article
- Astrocyte-neuron circuits in epilepsy.Neurobiology of disease · 2023Review
- Loss of maturity and homeostatic functions in Tuberous Sclerosis Complex-derived astrocytes.Frontiers in cellular neuroscience · 2023Article
- Mice deficient in complement C3 are protected against recognition memory deficits and astrogliosis induced by status epilepticus.Frontiers in molecular neuroscience · 2023Article
- Expression profiles of α-synuclein in cortical lesions of patients with FCD IIb and TSC, and FCD rats.Frontiers in neurology · 2023Article
- Astrocytes in the initiation and progression of epilepsy.Nature reviews. Neurology · 2022Review
Corrections and comments
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Authors and funding
19 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveIncreasing evidence supports the contribution of inflammatory mechanisms to the neurological manifestations of epileptogenic developmental pathologies linked to mammalian target of rapamycin (mTOR) pathway dysregulation (mTORopathies), such as tuberous sclerosis complex (TSC) and focal cortical dysplasia (FCD). In this study, we aimed to investigate the expression pattern and cellular distribution of the complement factors C1q and C3 in resected cortical tissue of clinically well-characterized patients with TSC and FCD2B.
methodsWe applied immunohistochemistry in TSC (n = 29) and FCD2B (n = 32) samples and compared them to autopsy and biopsy controls (n = 27). Furthermore, protein expression was observed via Western blot, and for descriptive colocalization studies immunofluorescence double labeling was performed.
resultsProtein expression for C3 was significantly upregulated in TSC and FCD2B white and gray matter lesions compared to controls. Staining of the synaptic vesicle protein synaptophysin showed a remarkable increase in the white matter of both TSC and FCD2B. Furthermore, confocal imaging revealed colocalization of complement factors with astroglial, microglial, neuronal, and abnormal cells in various patterns. SIGNIFICANCE: Our results demonstrate that the prominent activation of the complement pathway represents a common pathological hallmark of TSC and FCD2B, suggesting that complement overactivation may play a role in these mTORopathies.
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