Evolutionary mismatch hypothesis

Evolutionary Mismatch Hypothesis enters the Adult Cognitive Disease corpus through the work of Philip De Jager (submission 157), and is indexed here as one of the concepts that submission puts to work.

The argument it belongs to

Philip De Jager's submission is summarised in this corpus as:

AD is best understood as a mosaic of the aging brain driven by entropy, where the cause is systemic failure of brain function with the most common path involving amyloid and tau proteinopathy. AD risk is fundamentally modifiable, with genetic variants repurposed from early-life functions becoming pathogenic in later life contexts.

Where it sits

The submission scores against the framework's convergence nodes as: neuroimmune interface 7 · ApoE4 hub 7 · transcriptional / epigenetic 7 · endosomal nexus 5 · cytoskeletal collapse 3 · compensatory paradigm 3.

Its declared subject matter: SorLA-ER-homeostasis, microglial-CSF-proteomics, HEXIM1-transcription, P-TEFb, systems-biology, entropy, aging, GWAS, epigenomics, microglia, APOE, modifiable-risk.

Named by the same submission

6 other concepts enter the corpus through the same paper, so they cover adjacent ground: Entropy as organizing principle · Modifiability of AD risk · Mosaic model of aging brain · SorLA Lipid ER Regulation · Microglial Protein Biomarkers · Transcriptional Pause Release.

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.