Inflammaging integrates hallmarks of aging

Inflammaging Integrates Hallmarks Of Aging enters the Adult Cognitive Disease corpus through the work of Eduardo Chini (submission 127), and is indexed here as one of the concepts that submission puts to work.

The argument it belongs to

Eduardo Chini's submission is summarised in this corpus as:

Alzheimer's disease is driven by NAD metabolic dysfunction, an emerging hallmark of aging. The 'inflammaging' process leads to accumulation of senescent cells expressing CD38, which consume NAD+ and trigger a cascade of cellular dysfunctions that promote amyloid accumulation as part of a sterile inflammatory and anti-microbial response.

Where it sits

The submission scores against the framework's convergence nodes as: compensatory paradigm 7 · neuroimmune interface 7 · transcriptional / epigenetic 4 · ApoE4 hub 2 · endosomal nexus 1 · cytoskeletal collapse 1.

Its declared subject matter: NAD metabolism, inflammaging, cellular senescence, SASP, antimicrobial peptides, aging, sterile inflammation, CD38, immunometabolic-checkpoint, CD38-NADase, senescent-macrophage, bioenergetic-collapse.

Named by the same submission

4 other concepts enter the corpus through the same paper, so they cover adjacent ground: Aging as root cause of AD · Amyloid-beta as innate immune defense · NAD+ depletion drives neurodegeneration · Cellular Senescence.

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.