The renin-angiotensin system (RAS) is dysregulated in Alzheimer's disease (AD). In this study, we have explored the hypothesis that an age-related imbalance in brain RAS is a trigger for RAS dysregulation in AD. We characterised RAS gene expression in the frontal cortex from (i) a cohort of normal ageing (n = 99, age range = 19-96 y) and (ii) a case-control cohort (n = 209) including AD (n = 66), mixed dementia (VaD + AD) (n = 50), pure vascular dementia (VaD) (n = 42), and age-matched controls (n = 51). The AD, mixed dementia, and age-matched controls were further stratified by Braak tangle stage (BS): BS0-II (n = 48), BSIII-IV (n = 44) and BSV-VI (n = 85). Gene expression (qPCR) was calculated for ACE1, AGTR1, AGTR2, ACE2, LNPEP, and MAS1 using the 2-∆∆Cq method, after adjustment for reference genes (RPL13 and UBE2D2) and cell-specific calibrator genes (NEUN, GFAP, PECAM). ACE1 and AGTR1 gene expression, markers of classical RAS signalling, and AGTR2 gene expression were elevated in normal ageing but markers of protective downstream regulatory RAS (rRAS) signalling, including ACE2, MAS1, and LNPEP were unchanged. In AD and mixed dementia, AGTR1 and AGTR2 gene expression were elevated in BSIII-IV and BSV-VI respectively. MAS1 gene expression was reduced at BSV-VI and was inversely related to parenchymal Aβ and tau load. LNPEP gene expression was specifically elevated in VaD. These data provide novel insights into RAS signalling in normal ageing and dementia.