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Poly(ADP-ribose) drives pathologic α-synuclein neurodegeneration in Parkinson’s disease.

I have corresponded with James Clement about the possibility that elevated PARP-1 activity may a primary cause of the decline of NAD+ during aging, because PARP-1 consumes NAD+ as a cofactor in its activity. This group reports that PARP-1 also apparently accelerates the formation of toxic alpha-synuclein, and in at least one model, PARP-1 inhibition or deletion could prevent alpha-synuclein toxicity. PARP-1 inhibition or deletion does not seem like an enduring solution, as it leaves us tinkering with metabolism instead of cleaning up damage. I do wonder why PARP-1 is upregulated during aging; perhaps if we address the cause of this upregulation, we could prevent these negative downstream effects.
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