ReviewFrontiers in neuroscience2026
Interaction between Poly(ADP-ribose) polymerase-1 and α-synuclein pathology in Parkinson's disease.
Review in Frontiers in neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
Poly(ADP-ribose) polymerase-1 (PARP-1) activation and α-synuclein (α-syn) aggregation are neuropathological hallmarks of Parkinson's disease. This review aims to summarize the extensive interplay between these two factors. PARP-1 induces conformational changes in α-syn through structural reorganization mediated by poly(ADP-ribose) (PAR). Stress conditions resulting from PARP-1 overactivation are involved in the post-transcriptional regulation of α-syn. Oxidative and nitrative stress triggered by PARP-1 overactivation participate in the post-translational modifications of α-syn. PAR also contributes to α-syn degradation pathways, thereby influencing α-syn levels. Conversely, α-syn indirectly promotes PARP-1-dependent cell death via reactive oxygen species (ROS), suggesting a possible link through cell death pathways. These findings indicate that intracellular PARP-1, its metabolic products, and α-syn are closely associated, leading to dopaminergic neuronal vulnerability and potentially creating a vicious cycle of toxicity in PD pathology.
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