Runaway synaptic modification hypothesis

Runaway synaptic modification hypothesis enters the Adult Cognitive Disease corpus through the work of Simone Hasselmo (submission 108), and is indexed here as one of the concepts that submission puts to work.

The argument it belongs to

Simone Hasselmo's submission is summarised in this corpus as:

AD is driven by runaway synaptic modification (RSM), where the failure of mechanisms separating memory encoding from retrieval leads to inappropriate Hebbian synaptic strengthening. This malignant process causes exponential growth of dysfunctional synaptic connections, hyperactivation, and eventual cell death, with amyloid plaques and tangles being secondary consequences.

The source paper puts the concept to work directly:

Cholinergic and GABAB presynaptic inhibition could prevent runaway synaptic modification Additional support for the runaway synaptic modification hypothesis is provided by extensive research linking AD with cholinergic dysfunction (Bartus et al., 1982; Contestabile, 2011).

Where it sits

The submission scores against the framework's convergence nodes as: compensatory paradigm 8 · cytoskeletal collapse 2 · endosomal nexus 1 · transcriptional / epigenetic 1.

Its declared subject matter: synaptic-plasticity, memory, Hebbian-learning, hyperactivation, computational-model, associative-memory, graphic-narrative.

Named by the same submission

3 other concepts enter the corpus through the same paper, so they cover adjacent ground: Amyloid as secondary to synaptic dysfunction · Computational models of associative memory · Memory encoding-retrieval interference.

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.