Lipid homeostasis as AD driver

Lipid homeostasis as AD driver enters the Adult Cognitive Disease corpus through the work of Jin Xu (submission 44), and is indexed here as one of the concepts that submission puts to work.

The argument it belongs to

Jin Xu's submission is summarised in this corpus as:

Blood lipids and proteins form tightly regulated co-expression modules that are strongly associated with AD phenotypes including brain atrophy, cognitive decline, and diagnosis. Using weighted gene correlation network analysis (WGCNA) of integrated lipidomic and proteomic blood data, specific lipid and protein modules enriched in phosphatidylethanolamines, phosphatidylcholines, triglycerides, and complement/inflammatory proteins are linked to AD endophenotypes and genetic risk loci.

Where it sits

The submission scores against the framework's convergence nodes as: neuroimmune interface 5 · ApoE4 hub 5 · endosomal nexus 2 · compensatory paradigm 2.

Its declared subject matter: systems biology, lipidomics, proteomics, WGCNA, blood biomarkers, brain atrophy, network analysis, AD risk loci.

Named by the same submission

3 other concepts enter the corpus through the same paper, so they cover adjacent ground: Blood-based lipid and protein module biomarkers · Innate immunity network dysregulation in AD · Multi-omics network approach to 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.

Source: kb/wiki/concepts/Lipid homeostasis as AD driver.md