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DNA damage activates PARPs that can use up to 90% of the cell's NAD+, which makes DNA repair heavily reliant on NAD+ availability

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Bacterial native amyloid monomeric CsgA protein augmented aggregation of -synuclein proto-fibrils but did not trigger the acceleration of -synuclein monomer to its oligomeric form, as no interaction occurred between CsgA and -synuclein monomer in vitro (Sampson et al., 2020)

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