ArticleThe Journal of biological chemistry2013
C1q-induced LRP1B and GPR6 proteins expressed early in Alzheimer disease mouse models, are essential for the C1q-mediated protection against amyloid-β neurotoxicity.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 2 of them syntheses that pooled it.
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Who cites it
106 citing papers in PubMed, 2 syntheses or guidelines pooled it, 160 citations in OpenAlex.
- C1q as a target molecule to treat human disease: What do mouse studies teach us?Frontiers in immunology · 2022Pooled it
- Pooled it
- Article
- Discovery of Small Molecule Ligands Targeting Orphan G Protein-Coupled Receptors GPR3, GPR6, and GPR12.Journal of medicinal chemistry · 2026Review
- The complement system in Alzheimer's disease: evaluating biomarker potential in a complex neuroimmune context.Journal of neuroinflammation · 2026Review
- Structural signature of plasma proteins classifies the status of Alzheimer's disease.Nature aging · 2026Article
- CD8Frontiers in immunology · 2026Review
- The complement cascade in Alzheimer's disease: modern implications of an ancient immune protagonist.Molecular neurodegeneration · 2025Review
- Diverse Transcriptional Alterations in V2a Propriospinal Neurons Following Spinal Cord Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Young adult microglial deletion of C1q reduces engulfment of synapses and prevents cognitive impairment in an aggressive Alzheimer's disease mouse model.bioRxiv : the preprint server for biology · 2025Article
- Dysregulations of C1QA, C1QB, C1QC and C5AR1 as candidate biomarkers of vascular dementia.npj aging · 2025Article
- Knowing the enemy: strategic targeting of complement to treat Alzheimer disease.Nature reviews. Neurology · 2025Review
- The manipulator behind "Scissors": γ -secretase and its modulators in Alzheimer's disease.Frontiers in aging neuroscience · 2025Review
- Molecular pathogenesis of Alzheimer's disease onset in a mouse model: effects of cannabidiol treatment.Frontiers in neuroscience · 2025Article
- Music elicits different gene expression responses in the buccal cavity of age-related cognitive disorders patients and healthy controls.Frontiers in aging neuroscience · 2025Article
- Genetic variants associated with age-related episodic memory decline implicate distinct memory pathologies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Intracellular C1q - an unexpected player in neuronal proteostasis.Trends in immunology · 2024Article
- Review
- C5aR1 antagonism suppresses inflammatory glial responses and alters cellular signaling in an Alzheimer's disease mouse model.Nature communications · 2024Article
- Beneficial versus Detrimental Effects of Complement-Microglial Interactions in Alzheimer's Disease.Brain sciences · 2024Review
46 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Complement protein C1q is induced in the brain in response to a variety of neuronal injuries, including Alzheimer disease (AD), and blocks fibrillar amyloid-β (fAβ) neurotoxicity in vitro. Here, we show that C1q protects immature and mature primary neurons against fAβ toxicity, and we report for the first time that C1q prevents toxicity induced by oligomeric forms of amyloid-β (Aβ). Gene expression analysis reveals C1q-activated phosphorylated cAMP-response element-binding protein and AP-1, two transcription factors associated with neuronal survival and neurite outgrowth, and increased LRP1B and G protein-coupled receptor 6(GPR6) expression in fAβ-injured neurons. Silencing of cAMP-response element-binding protein, LRP1B or GPR6 expression inhibited C1q-mediated neuroprotection from fAβ-induced injury. In addition, C1q altered the association of oligomeric Aβ and fAβ with neurons. In vivo, increased hippocampal expression of C1q, LRP1B, and GPR6 is observed as early as 2 months of age in the 3 × Tg mouse model of AD, whereas no such induction of LRP1B and GPR6 was seen in C1q-deficient AD mice. In contrast, expression of C1r and C1s, proteases required to activate the classical complement pathway, and C3 showed a significant age-dependent increase only after 10-13 months of age when Aβ plaques start to accumulate in this AD model. Thus, our results identify pathways by which C1q, up-regulated in vivo early in response to injury without the coordinate induction of other complement components, can induce a program of gene expression that promotes neuroprotection and thus may provide protection against Aβ in preclinical stages of AD and other neurodegenerative processes.
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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 OpenQuestion graph.