Here is the relevant portion of the annual report (Baker IDI Heart and Diabetes Institute and impaired mitochondrial function due to metal dyshomeostasis) in case anyone missed it:
"In addition to impacting on protein targets such as tau, Abeta and alpha-synuclein, MPACs can modulate those metal dependent cellular biochemical processes that are compromised in the diseased neurodegenerative state. For example, metal dyshomeostasis in the brain has been shown to result in impaired cellular signaling and energy production. Indeed, impairment of the function of mitochondria, the cellular "power stations" has been implicated in the pathological process across the spectrum of neurodegenerative disease. (Johri and Flint-Beal, J Pharmacol Exp Ther-2012). Metals, especially copper and iron are crucial components of the energy production apparatus and dysregulation of the trafficking of these metals causes cellular energy deficits. Prana has entered a collaboration with scientists at the Baker IDI Heart and Diabetes Institute to employ Seahorse Extracellular Flux (XFÓ) microassay technology to assess the effect of novel Prana drugs on
mitochondrial function (respiration – oxygen consumption and glycolytic capacity) in a model of oxidative stress in cultured neurons."
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