Alzheimer’s disease (AD) is a devastating neurodegenerative disease and the main cause of dementia. This progressive disease is characterized by cognitive decline and is associated with brain atrophy and formation of amyloid plaques and neurofibrillary tangles. The production of amyloid-ß (Aß) is the key factor driving the pathology. Aß is highly toxic and leads to oxidative stress and neuroinflammation. Oxidative stress causes DNA damage such as the conversion of guanine to 8-oxoguanine (8-oxoG). The glycosylase that is mainly responsible for the repair of 8-oxoG is OGG1 which is encoded in the gene Ogg1. Although the impact of Ogg1 on DNA repair is well understood, its potential role in regulation of neuroinflammation and especially its impact on microglia in AD is yet to be investigated. We therefore examined the role of Ogg1 in regulation of neuroinflammation in AD using an Ogg1-knockout AD mouse model. We found that loss of Ogg1 leads to an altered ratio of amyloid species indicating increased toxicity as well as age-dependent changes in the inflammatory response. The loss of Ogg1 might contribute to impaired removal of toxic amyloid species in AD. Overall our findings indicate that OGG1 does play a role in the regulation of neuroinflammation in AD.