Expanded Prion Paradigm

Expanded Prion Paradigm enters the Adult Cognitive Disease corpus through the work of Stanley Prusiner (submission 142), and is indexed here as one of the concepts that submission puts to work.

The argument it belongs to

Stanley Prusiner's submission is summarised in this corpus as:

Alzheimer's disease is a double prion disorder caused by the self-propagating misfolding of both Abeta and tau proteins. Prion bioassays reveal that biologically active (infectious) prion forms of Abeta and tau decrease with age while insoluble inert forms accumulate, and that tau prion infectivity rather than total tau burden correlates with disease severity and longevity.

Where it sits

The submission scores against the framework's convergence nodes as: cytoskeletal collapse 5 · endosomal nexus 2 · compensatory paradigm 1.

Its declared subject matter: prion-paradigm-expansion, protein-misfolding-diseases, synuclein-prions, prion disease, protein misfolding, tau prions, Abeta prions, prion bioassay, transmissibility, anti-prion therapeutics, double prion disorder.

Use in the corpus

Referred to by 1 document in the research corpus, including research/collapse-trilogy/PhD_Thesis_Vagal_Interface.md.

Named by the same submission

5 other concepts enter the corpus through the same paper, so they cover adjacent ground: AD as a double prion disorder · Anti-prion therapeutics as novel drug strategy · Prion infectivity distinct from insoluble protein accumulation · Tau prions drive disease more than Abeta prions · Cross Disease Prion Mechanisms.

Related

Adrenergic Signaling · Autophagy · Axonal Transport · Bioenergetic Collapse · Convergent Synaptic Collapse

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; the reference count is measured across the research corpus. It has not yet been expanded into an article.