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In this paper, we explore the potential role of certain amyloidogenic proteins, including amylin, amyloid beta, the prion protein, huntingtin, and -synuclein, in disease processes that result in the accumulation of deposits of protein fibrils, along with lipid membrane components of damaged mitochondria, which we argue may be a mechanism to sequester deuterium in order to reduce the deuterium burden in the tissues
Doxorubicin (DOX)-induced cardiomyopathy (DIC) A study by Fang et al
Harris JA, Faust B, Gondin AB et al (2022) Selective G protein signaling driven by substance Pneurokinin receptor dynamics
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