ATP depletion as direct trigger of tau pathology

Atp Depletion As Direct Trigger Of Tau Pathology enters the Adult Cognitive Disease corpus through the work of Günter Höglinger (submission 140), and is indexed here as one of the concepts that submission puts to work.

The argument it belongs to

Günter Höglinger's submission is summarised in this corpus as:

Environmental toxins acting as mitochondrial complex I (CxI) inhibitors are etiological factors in Alzheimer's disease and other tauopathies. Annonacin and other natural CxI inhibitors cause ATP depletion, which triggers tau redistribution from axons to the somatodendritic compartment, hyperphosphorylation, and neuronal cell death in a dose-dependent manner.

Where it sits

The submission scores against the framework's convergence nodes as: cytoskeletal collapse 8 · compensatory paradigm 2.

Its declared subject matter: environmental toxins, mitochondrial complex I, tauopathy, annonacin, ATP depletion, tau redistribution, Guadeloupe parkinsonism, rotenone, energy-gate-mechanism, axonal-transport-failure, bioenergetic-collapse, PSP.

Named by the same submission

3 other concepts enter the corpus through the same paper, so they cover adjacent ground: Dietary neurotoxin exposure as modifiable risk factor · Dose-dependent mitochondrial dysfunction determines pathology type · Environmental CxI inhibitors as AD etiological agents.

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.