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Kam, Tae-In; Mao, Xiaobo; Park, Hyejin; Chou, Shih-Ching; Karuppagounder, Senthilkumar S; Umanah, George Essien; Yun, Seung Pil; Brahmachari, Saurav; Panicker, Nikhil; Chen, Rong; Andrabi, Shaida A; Qi, Chen; Poirier, Guy G; Pletnikova, Olga; Troncoso, Juan C; Bekris, Lynn M; Leverenz, James B; Pantelyat, Alexander; Ko, Han Seok; Rosenthal, Liana S; Dawson, Ted M; Dawson, Valina L
Science (American Association for the Advancement of Science), 11/2018, Letnik: 362, Številka: 6414Journal Article
The pathologic accumulation and aggregation of α-synuclein (α-syn) underlies Parkinson's disease (PD). The molecular mechanisms by which pathologic α-syn causes neurodegeneration in PD are not known. Here, we found that pathologic α-syn activates poly(adenosine 5'-diphosphate-ribose) (PAR) polymerase-1 (PARP-1), and PAR generation accelerates the formation of pathologic α-syn, resulting in cell death via parthanatos. PARP inhibitors or genetic deletion of PARP-1 prevented pathologic α-syn toxicity. In a feed-forward loop, PAR converted pathologic α-syn to a more toxic strain. PAR levels were increased in the cerebrospinal fluid and brains of patients with PD, suggesting that PARP activation plays a role in PD pathogenesis. Thus, strategies aimed at inhibiting PARP-1 activation could hold promise as a disease-modifying therapy to prevent the loss of dopamine neurons in PD.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Povezave do osebnih bibliografij avtorjev | Povezave do podatkov o raziskovalcih v sistemu SICRIS |
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Vir: Osebne bibliografije
in: SICRIS
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