Parkinson’s disease (PD) is a neurodegenerative disorder that is mainly characterised by the loss of dopaminergic neurons in the substantia nigra as well as the presence of aggregates called Lewy bodies which consist mostly of alpha-synuclein. Astrocytes and microglia are increasingly being regarded as key players in PD-associated neurodegeneration, and these become ‘activated’ during neuroinflammation. Autophagy and its dysfunction have been implicated in some genetic forms of PD, with alpha-synuclein accumulation and aggregation linked to autophagy suppression. Using alpha-synuclein triplication mutant and control hiPSC-derived ventral midbrain astrocytes (vmAstros) and microglia, we are testing the effects of autophagy modulation on inflammatory signalling in these cells. Using an inflammatory cocktail of IL-1alpha, TNFalpha and C1q (ITC), we induce vmAstros reactivity in vitro, with chemical autophagy modulators (e.g., trehalose; bafilomycin A1), and genetic tools (overexpression of dominant negative of ATG4BC74A), we will present secretomics data on the interplay between autophagy and neuroinflammation, with further biochemical assays describing how neuroinflammation itself can modulate the autophagy response. These data will contribute to a better appreciation of the crosstalk between glial cells in a hiPSC Parkinson’s model, and insights will expand our current understanding of the changes occurring in the early stages of PD.