Denervation supersensitivity

Denervation Supersensitivity enters the Adult Cognitive Disease corpus through the work of Christoph Methfessel (submission 79), and is indexed here as one of the concepts that submission puts to work.

The argument it belongs to

Christoph Methfessel's submission is summarised in this corpus as:

Alzheimer's disease is fundamentally caused by impaired cholinergic neurotransmission, with amyloid plaques and tau tangles being secondary consequences rather than primary causes. Denervation supersensitivity in postsynaptic neurons causes them to revert to a juvenile biochemical state, overproducing APP and tau, which then accumulate as plaques and tangles.

The source paper puts the concept to work directly:

This would counteract denervation supersensitivity, and thus prevent the excess production of APP and tau. The therapeutic goal would therefore be to activate (or possibly desensitize) the nAChRs on these neurons by substituting ACh with a drug that supplies a similar signal to the α7 nAChR subtype.

Where it sits

The submission scores against the framework's convergence nodes as: compensatory paradigm 7 · cytoskeletal collapse 3 · transcriptional / epigenetic 2 · neuroimmune interface 1.

Its declared subject matter: cholinergic-hypothesis, denervation-supersensitivity, nicotinic-receptors, synaptic-plasticity, amyloid-secondary, nAChR, neurotransmission, therapeutic-targets.

Named by the same submission

3 other concepts enter the corpus through the same paper, so they cover adjacent ground: Amyloid and tau as secondary phenomena · Cholinergic primacy in AD · Receptor-based therapeutic approach.

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