ReviewJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2023
As a Potential Therapeutic Target, C1q Induces Synapse Loss Via Inflammasome-activating Apoptotic and Mitochondria Impairment Mechanisms in Alzheimer's Disease.
Review in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Cardiopulmonary crosstalk in Long COVID: a systematic review of emerging evidence.BMC cardiovascular disorders · 2025Pooled it
- Exploration of the genetic neuroinflammatory environment in the human midcingulate cortex in Huntington's disease.Communications medicine · 2026Article
- Emerging pathological mechanisms of Alzheimer's disease pathogenesis: from neuroimmune interactions to intercellular communication.Frontiers in aging neuroscience · 2026Review
- [C1q-neutralizing antibodies improves postpartum depressive-like behaviors in mice by regulating the C1q/C3 pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Complement C1q is associated with neuroinflammation and mediates the association between amyloid-β and tau pathology in Alzheimer's disease.Translational psychiatry · 2025Article
- Hyaluronan: An Architect and Integrator for Cancer and Neural Diseases.International journal of molecular sciences · 2025Review
- Targeted demethylation of cathepsin D via epigenome editing rescues pathology in Alzheimer's disease mouse model.Theranostics · 2025Article
- NLRP12/C1qA positive feedback in tumor-associated macrophages regulates immunosuppression through LILRB4/NF-κB pathway in lung adenocarcinoma.Cancer immunology, immunotherapy : CII · 2024Article
- The PANoptosis-related hippocampal molecular subtypes and key biomarkers in Alzheimer's disease patients.Scientific reports · 2024Article
- Double-Edged Sword: Exploring the Mitochondria-Complement Bidirectional Connection in Cellular Response and Disease.Biology · 2024Review
- Metabolic regulation of microglial phagocytosis: Implications for Alzheimer's disease therapeutics.Translational neurodegeneration · 2023Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
C1q, the initiator of the classical pathway of the complement system, is activated during Alzheimer's disease (AD) development and progression and is especially associated with the production and deposition of β-amyloid protein (Aβ) and phosphorylated tau in β-amyloid plaques (APs) and neurofibrillary tangles (NFTs). Activation of C1q is responsible for induction of synapse loss, leading to neurodegeneration in AD. Mechanistically, C1q could activate glial cells, which results in the loss of synapses via regulation of synapse pruning and phagocytosis in AD. In addition, C1q induces neuroinflammation by inducing proinflammatory cytokine secretion, which is partially mediated by inflammasome activation. Activation of inflammasomes might mediate the effects of C1q on induction of synapse apoptosis. On the other hand, activation of C1q impairs mitochondria, which hinders the renovation and regeneration of synapses. All these actions of C1q contribute to the loss of synapses during neurodegeneration in AD. Therefore, pharmacological, or genetic interventions targeting C1q may provide potential therapeutic strategies for combating AD.
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