Tat-treated BV-2 cells cultured with primary axons contain inclusions of neuronal components that are altered by LRRK2 kinase inhibition. We immunostained BV-2-neuronal cultures for the axonal cytoskeletal protein Tau 5 (green), the axonal terminal protein Synapsin-1 (red), and the microglial membrane protein CD11b (light blue) after 18 hours of experimental treatment. Saline (A) and DMSO (B) treated BV-2 cells do not appear to phagocytose any neuronal components. Tat treated BV-2 cells (C, D, E) contain Tau-5 and Synapsin-1 positive inclusions, indicative of axonal phagocytosis (white arrows). Tat exposed BV-2 cells treated with LRRK2i (F) contain some neuronal inclusions that are much smaller than Tat exposed alone (white arrowheads), indicating a stunted phagocytic process. Tat exposed BV-2 cells treated with AnnexinV (G) contain fewer inclusions than Tat alone, but the inclusions are the same size as the Tat alone treated condition (white arrows). LRRK2i, leucine-rich repeat kinase 2 inhibitor; Tat, trans activator of transcription.