Mitochondrial theory of aging

Mitochondrial Theory Of Aging enters the Adult Cognitive Disease corpus through the work of Anne Eckert (submission 95), and is indexed here as one of the concepts that submission puts to work.

The argument it belongs to

Anne Eckert's submission is summarised in this corpus as:

AD in women is triggered by the neuroendocrine and bioenergetic shift at menopause, where the sudden drop in estradiol compromises mitochondrial function, redox homeostasis, and brain energy metabolism. Age-related mitochondrial dysfunction creates a vicious cycle of oxidative stress and Abeta/tau pathology, with women being especially vulnerable due to loss of estradiol's neuroprotective effects on OxPhos.

The source paper puts the concept to work directly:

Mitochondrial theory of aging a. Free-radicals theory of aging The “free-radicals theory of aging” was stated for the first time by Harman in 19569, and postulates that aging, as well as age-associated degenerative diseases, is a consequence of free radicals attacks on cells and tissues.

Where it sits

The submission scores against the framework's convergence nodes as: neuroimmune interface 4 · compensatory paradigm 3 · transcriptional / epigenetic 3 · cytoskeletal collapse 2 · ApoE4 hub 2 · endosomal nexus 1.

Its declared subject matter: mitochondrial-dysfunction, menopause, sex-hormones, oxidative-stress, bioenergetics, estradiol, women-and-AD, redox-homeostasis.

Named by the same submission

3 other concepts enter the corpus through the same paper, so they cover adjacent ground: Bioenergetic defects as early events · Neuroendocrine shift at menopause · Sex-specific AD vulnerability.

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. It has not yet been expanded into an article.