Excitatory Neurotransmission

Excitatory Neurotransmission 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.

The source paper puts the concept to work directly:

Keywords Compensatory response, excitatory neurotransmission, neuronal development, NMDA receptor. 1 Section 1. Major risk factors for hereditary and sporadic AD share the inhibition of excitatory neurotransmission as immediate consequence (Figure 1) Five well-established, independent risk factors for AD were chosen for hypothesis generation.

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.

Use in the corpus

Referred to by 2 documents in the research corpus, including research/collapse-trilogy/convergent-synaptic/ONS_SynapticCollapse_Thesis.md, research/excitation-inhibition/PhD_Thesis_Low_Signal_High_Noise.md.

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 · Compensatory Homeostasis · Lysosomal Acidification · Synaptic Pathology · Synaptic Physiology.

Related

cognitive resilience · Convergent Synaptic Collapse · Oskar Fischer Founder

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; the reference count is measured across the research corpus. It has not yet been expanded into an article.