This paper explore the cellular response to the stress that Deuterium caused in the cells. It shed some light on the potential role of certain amyloid proteins (like amyloid beta), the prion protein, huntingtin, and α-synuclein, in disease processes. The results is the accumulation of deposits of protein fibrils, along with lipid membrane components of damaged mitochondria, which may be argues as the mechanism the body devised to sequester deuterium in order to reduce the deuterium burden in the tissues.