Neuroinflammation as primary driver connecting all AD subsystems

Neuroinflammation As Primary Driver Connecting All Ad Subsystems enters the Adult Cognitive Disease corpus through the work of David Gate (submission 139), and is indexed here as one of the concepts that submission puts to work.

The argument it belongs to

David Gate's submission is summarised in this corpus as:

Alzheimer's disease is a systems-level disorder where antiviral neuroinflammation is the primary driver, connecting all three pathological subsystems (amyloid plaques, neurofibrillary tangles, neuroinflammation). Viral infections exploit age-related immunosenescence to infect the brain, triggering chronic neuroinflammation that drives both Abeta production/accumulation and tau hyperphosphorylation.

Where it sits

The submission scores against the framework's convergence nodes as: neuroimmune interface 9 · compensatory paradigm 6 · ApoE4 hub 3 · endosomal nexus 2 · transcriptional / epigenetic 2 · cytoskeletal collapse 1.

Its declared subject matter: neuroinflammation, viral infection, systems biology, NLRP3 inflammasome, immunosenescence, microglia, complement system, antiviral response, effector-triad, C5a-C5aR, TREM2-NLRP3-coupling, single-cell-microglia.

Named by the same submission

4 other concepts enter the corpus through the same paper, so they cover adjacent ground: Age-related immune dysfunction enables neurotropic viruses · Systems approach to interconnected AD pathological hallmarks · Viral infection triggers chronic brain inflammation · Cellular Senescence.

Assembled from the corpus rather than written: the summary is quoted from the submission that named it; the node scores are read from its dossier. It has not yet been expanded into an article.