Adult Cognitive DiseaseThe research corpus Monographs

Neuroimmune Interface

Microglial-complement pruning cascade that accelerates synaptic loss through immune-mediated destruction.

Converging Mechanisms

  • C4d deposition on synapses triggers LilrB2 signaling (Shatz/Brott)
  • TREM2-mediated microglial phagocytosis of synapses
  • Pattern recognition of DAMPs (oxidized proteins, Abeta, pTau)
  • Trans-synaptic immune signaling triggers cytoskeletal collapse

Key Molecules

C1q, C3, C4d, LilrB2, TREM2, CR3

To be populated after CSC grading.

See Also

Papers converging on this axis

8
From Synapse Loss to Neuronal Death in Alzheimer's Disease 6 concepts · 6 genes shared The Losing Axon 6 concepts · 6 genes shared The Senescent Front 6 concepts · 4 genes shared Mapping the Vascular Dimension Onto the Genetic Dimension 5 concepts · 6 genes shared The Proteolytic Turn 5 concepts · 6 genes shared The Unified Architecture of Collapse 5 concepts · 6 genes shared The Complement-pruning Substrate 5 concepts · 5 genes shared The Viral Trajectory 5 concepts · 5 genes shared

Concepts on this axis

509
Abeta aggregation as necessary initiating eventAbeta as molecular prime moverAbeta as stress response markerActivated microglia imaging for treatment guidanceAcyloxyacyl Hydrolase NeuroprotectionAD as accelerated aging of Abeta managementAD as accumulation of insults exceeding homeostasisAD as autoimmune disorderAD as clinical syndrome not diseaseAD as systemic disease not limited to brainAD caused by APP dysregulation not Abeta per seAD-diabetes shared mechanismAdult hippocampal neurogenesis restorationAdult NeurogenesisAge-dependent feedback loops in neurodegenerationAge-dependent threshold modelAge-related immune dysfunction enables neurotropic virusesAging accelerators and deceleratorsAging as MechanismAging as root cause of ADAging-epigenetic-genetic interactionAI Neurotherapeutic DiscoveryAI-based early diagnosisAlpha-sheet toxicity in disease pathogenesisAluminum as primary environmental causeAluminum driving amyloid productionAmyloid and tau as secondary byproductsAmyloid and tau as secondary phenomenaAmyloid as antimicrobial defenseAmyloid as defense mechanism against parasitesAmyloid as downstream secondaryAmyloid as innate immune defense gone awryAmyloid clearance as important as depositionAmyloid Clinical DisconnectAmyloid NucleationAmyloid plaques as fibrotic scar tissue from BBB repairAmyloid-beta as innate immune defenseAnti Ferroptotic BotanicalsAnti-TNF-alpha therapeutic strategyAntibody Target Specificity
Source: kb/wiki/convergence-nodes/neuroimmune-interface.md