Sigma-1 receptor-mediated neuroprotection

Sigma-1 receptor-mediated neuroprotection enters the Adult Cognitive Disease corpus through the work of Jian-Sheng Kang (submission 30), and is indexed here as one of the concepts that submission puts to work.

The argument it belongs to

Jian-Sheng Kang's submission is summarised in this corpus as:

Brain atrophy and hypometabolism, driven by neuronal energy failure and defective autophagy, are causative factors of Alzheimer's disease rather than merely consequences. Fluoxetine, a selective serotonin reuptake inhibitor, may have strong therapeutic potential for AD through multiple mechanisms including promoting neurogenesis, enhancing BDNF expression, inhibiting secretase activity, and ameliorating hypometabolism via sigma-1 receptor activation and mitochondrial calcium signaling.

Where it sits

The submission scores against the framework's convergence nodes as: compensatory paradigm 4 · endosomal nexus 3 · neuroimmune interface 1 · transcriptional / epigenetic 1.

Its declared subject matter: hypometabolism, autophagy, fluoxetine, SSRI, brain atrophy, neurogenesis, BDNF, gamma-secretase.

Named by the same submission

3 other concepts enter the corpus through the same paper, so they cover adjacent ground: Autophagy-metabolism crosstalk in AD · Energy failure as primary AD driver · SSRI repurposing for neurodegeneration.

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.