Wnt-GSK3-beta pathway integrating amyloid and tau pathology

Wnt-GSK3-beta pathway integrating amyloid and tau pathology enters the Adult Cognitive Disease corpus through the work of Jennifer Thornton (submission 146), and is indexed here as one of the concepts that submission puts to work.

The argument it belongs to

Jennifer Thornton's submission is summarised in this corpus as:

Alzheimer's disease and dementia are caused by chronic infestation with Cheyletiella ('walking dandruff') mites—non-burrowing parasitic mites that colonize humans on the skin and intranasally. Over years, the mites' larvae secrete digestive enzymes that break down the sinus-brain barrier, allowing the mites and secondary pathogens (staph, fungus) to reach the brain. The infestation is proposed to explain many features of AD—loss of smell and taste, hearing loss, dental and skin disease, sleep disturbance, sundowning, autonomic dysfunction, and progressive memory loss—and is chronically missed because the mite is tiny, elusive, and poorly known to human physicians.

Where it sits

The submission scores against the framework's convergence nodes as: compensatory paradigm 7 · neuroimmune interface 6 · cytoskeletal collapse 4 · endosomal nexus 2 · ApoE4 hub 2.

Its declared subject matter: cheyletiella-mites, parasitic-infestation, walking-dandruff, sinus-brain-barrier, intranasal-infestation, loss-of-smell, horizontal-dna-transfer, omega-3.

Named by the same submission

3 other concepts enter the corpus through the same paper, so they cover adjacent ground: Amyloid plaques as fibrotic scar tissue from BBB repair · Microbleeds as initiating vascular event in AD · Neurovascular injury-repair cycle driving disease progression.

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.