Calcium dyshomeostasis as upstream AD mechanism

Calcium dyshomeostasis as upstream AD mechanism enters the Adult Cognitive Disease corpus through the work of Leandro Bergantin (submission 45), and is indexed here as one of the concepts that submission puts to work.

The argument it belongs to

Leandro Bergantin's submission is summarised in this corpus as:

Age-related deregulation of neuronal calcium (Ca2+) homeostasis is a central upstream mechanism driving Alzheimer's disease. Abeta accumulation disrupts Ca2+ signaling through voltage-activated calcium channels (VACC) and ER calcium stores, creating a vicious cycle of excitotoxicity. L-type calcium channel blockers (CCBs) such as isradipine, combined with phosphodiesterase inhibitors, represent a promising pharmacological strategy to modulate Ca2+/cAMP signaling and provide neuroprotection.

Where it sits

The submission scores against the framework's convergence nodes as: compensatory paradigm 3 · endosomal nexus 2 · cytoskeletal collapse 1 · neuroimmune interface 1.

Its declared subject matter: calcium signaling, calcium channel blockers, VACC, excitotoxicity, hypertension, neuroprotection, isradipine, cAMP.

Named by the same submission

3 other concepts enter the corpus through the same paper, so they cover adjacent ground: Ca2+-cAMP signaling convergence in neurodegeneration · L-type CCB neuroprotective strategy · Repurposing antihypertensives for AD.

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.