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The Classical Complement Cascade Mediates CNS Synapse Elimination

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Last updated 25 fevereiro 2025
The Classical Complement Cascade Mediates CNS Synapse Elimination
The Classical Complement Cascade Mediates CNS Synapse Elimination
As a Potential Therapeutic Target, C1q Induces Synapse Loss Via Inflammasome-activating Apoptotic and Mitochondria Impairment Mechanisms in Alzheimer's Disease
The Classical Complement Cascade Mediates CNS Synapse Elimination
Full article: The case for complement component 5 as a target in neurodegenerative disease
The Classical Complement Cascade Mediates CNS Synapse Elimination
Biomedicines, Free Full-Text
The Classical Complement Cascade Mediates CNS Synapse Elimination
C1q: the perfect complement for a synaptic feast?
The Classical Complement Cascade Mediates CNS Synapse Elimination
Glia, Neurobiology Journal
The Classical Complement Cascade Mediates CNS Synapse Elimination
Frontiers Complement Activation in the Central Nervous System: A Biophysical Model for Immune Dysregulation in the Disease State
The Classical Complement Cascade Mediates CNS Synapse Elimination
Microglial trogocytosis and the complement system regulate axonal pruning in vivo
The Classical Complement Cascade Mediates CNS Synapse Elimination
Complement C3-dependent glutamatergic synapse elimination in the developing hippocampus is region- and synapse-specific
The Classical Complement Cascade Mediates CNS Synapse Elimination
The Classical Complement Cascade Mediates CNS Synapse Elimination: Cell
The Classical Complement Cascade Mediates CNS Synapse Elimination
Figure 2 from The complement system: an unexpected role in synaptic pruning during development and disease.
The Classical Complement Cascade Mediates CNS Synapse Elimination
A new age for (mucosal) NeuroImmunology - Mucosal Immunology
The Classical Complement Cascade Mediates CNS Synapse Elimination
Complement and microglia mediate early synapse loss in Alzheimer mouse models
The Classical Complement Cascade Mediates CNS Synapse Elimination
Mechanisms governing activity-dependent synaptic pruning in the developing mammalian CNS
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