Compensatory Homeostasis

Compensatory Homeostasis enters the Adult Cognitive Disease corpus through the work of Bernd Moosmann (submission 145), and is indexed here as one of the concepts that submission puts to work.

The argument it belongs to

Bernd Moosmann's submission is summarised in this corpus as:

Chronic excitatory insufficiency—the inhibition of glutamatergic, NMDA-receptor-mediated neurotransmission—is the common molecular denominator shared by five maximally disparate AD risk factors (ApoE4, Presenilin 1 mutations, menopausal estrogen loss, mechanical neurotrauma, and Trisomy 21) and the proximate cause of Alzheimer's disease. Suppressed excitatory neurotransmission accounts for the main phenotype (learning and memory failure) and minor phenotypes (sleep disturbance, hearing loss, agitation, silent seizures). Amyloid-beta formation and tau phosphorylation are rapidly induced by excitatory insufficiency and act as purposeful, compensatory enhancers of excitatory neurotransmission rather than primary toxins.

Where it sits

The submission scores against the framework's convergence nodes as: compensatory paradigm 9 · endosomal nexus 8 · ApoE4 hub 8 · cytoskeletal collapse 2 · neuroimmune interface 1 · transcriptional / epigenetic 1.

Its declared subject matter: excitatory-insufficiency, glutamatergic-neurotransmission, nmda-receptor, compensatory-response, risk-factor-convergence, apoe4, presenilin-1, amyloid-as-compensation.

Named by the same submission

7 other concepts enter the corpus through the same paper, so they cover adjacent ground: Axonal Transport · Calcium Homeostasis · Chronic Excitatory Insufficiency · Excitatory Neurotransmission · Lysosomal Acidification · Synaptic Pathology · Synaptic Physiology.

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.