Tau as conditional prion

Tau As Conditional Prion enters the Adult Cognitive Disease corpus through the work of Hanno Roder (submission 63), and is indexed here as one of the concepts that submission puts to work.

The argument it belongs to

Hanno Roder's submission is summarised in this corpus as:

Alzheimer's disease is dominated by tau as a conditional prion. Tau pathology, not amyloid, drives irreversible neurodegeneration, and the disease spreads through prion-like propagation of abnormally modified tau along neural pathways. The failure of amyloid-focused therapies stems from conflating reversible synaptic effects of Abeta with the irreversible neurodegeneration caused by tauopathy.

Where it sits

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

Its declared subject matter: tauopathy, prion-like-propagation, tau-phosphorylation, tau-splicing, neurodegeneration, anti-amyloid-critique, conditional-prion, neuronal-maturation.

Named by the same submission

3 other concepts enter the corpus through the same paper, so they cover adjacent ground: Neuronal maturation context in disease · Post-translational modification as prion trigger · Tauopathy primacy over amyloidopathy.

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.