Twin publications in npj Parkinson’s Disease report that protein glycation increases alpha‑synuclein aggregation and heightens neuroinflammatory responses in models relevant to Parkinson’s disease. The studies link metabolic alterations to pathogenic protein chemistry and downstream immune activation. Authors show that glycation products promote fibril formation and exacerbate microglial responses, suggesting metabolic control could alter disease biology. The papers propose glycation as a modifiable mechanism that intersects proteinopathy and neuroinflammation. For translational teams: the findings point to metabolic interventions and anti‑glycation strategies as candidate adjuncts to protein‑targeting therapies and identify biomarkers for patient stratification in early trials.