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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

Retrieved from Tabrizi, R., Tamtaji, O

thus, alternative delivery methods have been investigated for anti-TNFs [183]

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This dual mechanism approach allows researchers to examine whether combined pathway activation produces different metabolic effects compared to single-pathway targeting

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