Ferroptosis in Neurodegeneration

Ferroptosis In Neurodegeneration enters the Adult Cognitive Disease corpus through the work of Ashley Bush (submission 152), and is indexed here as one of the concepts that submission puts to work.

The argument it belongs to

Ashley Bush's submission is summarised in this corpus as:

The Ferroptosis Theory posits that Alzheimer's disease is fundamentally a disease of iron-dependent, non-apoptotic cell death (ferroptosis) driven by progressive age-related brain iron accumulation. Amyloid plaques and tau tangles are compensatory 'sinks' for toxic lipid aldehydes and redox-active iron, and FAD mutations in APP and PSEN1 are loss-of-function events that impair anti-ferroptotic defenses via a Presenilin-Notch-LRP8-GPX4 signaling axis.

Where it sits

The submission scores against the framework's convergence nodes as: compensatory paradigm 8 · endosomal nexus 5 · ApoE4 hub 2 · cytoskeletal collapse 1 · neuroimmune interface 1 · transcriptional / epigenetic 1.

Its declared subject matter: ferroptosis, iron-homeostasis, lipid-peroxidation, oxidative-stress, GPX4, presenilin, Notch-signaling, iron-chelation, aging, membrane-integrity, deferiprone-failure, PUFA-vulnerability.

Use in the corpus

Referred to by 2 documents in the research corpus, including research/iron-gpx4-pharmacology/Iron_GPX4_Pharmacology.md, research/therapeutic-landscape/papers/Ferroptosis_Phase_II_Oligodendrocyte.md.

Named by the same submission

6 other concepts enter the corpus through the same paper, so they cover adjacent ground: Ferroptosis · Iron Brain Paradox · Iron Dyshomeostasis · Lipid Peroxidation · Lysosomal Acidification · Oxidative Stress.

Related

Lipid Metabolism · Neuroinflammation · Oskar Fischer Founder · Autophagy

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