Optineurin is an adaptor protein implicated in multiple cellular processes, such as autophagy, vesicular trafficking, exocytosis, and inflammation. Mutations in the optineurin gene have been linked with amyotrophic lateral sclerosis (ALS), a neurodegenerative disease impacting motor neurons. Previous research has found that phagocytosis, the process of removing extracellular particles by professional phagocytic cells, was disrupted in ALS, and research from our laboratory on cell lines has shown slightly impaired phagocytosis in optineurin deficient cells. The goal of this thesis was to research the role of optineurin in phagocytosis using primary cells. To do that, we performed a flow cytometry-based assay on primary wild type (WT) and optineurin-insufficient OPTN470T bone marrow-derived macrophages (BMDMs) generated from mice aged 3 months and 2 years and microglia generated from neonatal mice. We found no difference between the genotypes in the number of phagocytic cells or their phagocytic ability in basal condition in neither BMDM nor microglia. The same lack of difference persisted when primary cells were pre-treated with inflammatory stimuli, as well as when degradation through autophagy and lysosomes was blocked. Interestingly, we found that phagocytosis was impaired in BMDMs from older mice compared to BMDMs from younger mice, but the difference was not significant when cells were pre-treated with an inflammatory stimulus. In conclusion, this study did not confirm the role of optineurin in phagocytosis of neuronal debris by primary cells, but the difference in the level of phagocytosis between cells generated from younger and older mice opens up a new route of research