Aims: This thesis aimed to investigate the relationship between memory errors and delusions in Alzheimer’s disease (AD), in order to further elucidate the mechanisms underlying delusion formation. This was achieved by undertaking narrative and systematic review of relevant literature, by exploring the relationship between performance on memory and metamemory tasks and delusions in AD patient populations and by investigating the neuroanatomical correlates of memory errors and delusions in AD patient populations. // Methods: I recruited 27 participants with and without delusions in AD and compared performance on measures of context memory, false memory and metamemory. I explored statistically significant behavioural findings further in the Alzheimer’s Disease Neuroimaging Initiative (ADNI) cohort of participants with AD (n = 733). I then conducted hypothesis-driven region of interest and exploratory voxel-based morphometric analyses to determine the relationship between false memory and delusions and regional brain volume in the ADNI cohort. This informed similar analyses of neuroimaging data in my own participants (n = 8). // Results: In both samples, individuals with delusions in AD had higher false recognition rates on recognition memory tasks than those without delusions. False recognition was inversely correlated with volume of medial temporal lobe, ventral visual stream and prefrontal cortex in both samples. In the ADNI sample, false recognition was also inversely correlated with anterior cingulate cortex (ACC) volume bilaterally. Participants with delusions had reduced volume of right ACC and increased volume of right parahippocampal gyrus compared to the control group. // Conclusions: These two complementary studies provide evidence of specific memory impairments associated with both delusions and a distinct pattern of brain atrophy in AD. Simple cognitive interventions can reduce false recognition rates in AD. Given the significant risks associated with antipsychotic drug treatment of delusions, exploring how these non-pharmacological interventions potentially affect psychosis symptoms in AD is an important next step
