Amyloid as innate immune defense gone awry

Amyloid As Innate Immune Defense Gone Awry enters the Adult Cognitive Disease corpus through the work of Philip Serwer (submission 41), and is indexed here as one of the concepts that submission puts to work.

The argument it belongs to

Philip Serwer's submission is summarised in this corpus as:

Amyloid-forming proteins like Abeta are protein versions of CRISPR phage sequences -- they are originally derived from virus-encoded proteins and function as part of an innate immune system that recognizes and neutralizes viruses by adopting beta-sheet structure. Neurodegenerative disease occurs when this innate immunity function becomes over-active, with neurons producing excessive alpha-sheet structured amyloid protein in a misguided attempt to neutralize already-inactivated threats. Herpesvirus infection may be a key trigger.

Where it sits

The submission scores against the framework's convergence nodes as: neuroimmune interface 8 · compensatory paradigm 6.

Its declared subject matter: innate immunity, viral etiology, protein structure, alpha-sheet, beta-sheet, CRISPR analogy, herpesvirus, bacteriophage.

Named by the same submission

3 other concepts enter the corpus through the same paper, so they cover adjacent ground: Alpha-sheet toxicity in disease pathogenesis · CRISPR-like protein immunity model · Viral trigger hypothesis for neurodegeneration.

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.