It has been suggested that aged and neuropsychiatric disease brains commonly share the possibility of increased inflammation due to increased retrotransposon cDNA. In this study, we will therefore elucidate mechanisms of how and which cell types in these brains enter an ageing state, induce brain inflammation and lead to brain dysfunction. Furthermore, using mouse, marmoset and human brain organoids, we will investigate whether the suppression of cDNA production can prevent the progression of brain function decline and whether rejuvenating the ageing cells can improve the decline in brain function.