Personality factors have been associated with Alzheimer’s disease (AD) and dementia, but they have not been examined against markers of regional brain glucose metabolism (a primary measure of brain functioning) in older adults without clinically diagnosed cognitive impairment. The relationship between personality factors derived from the five-factor model and cerebral glucose metabolism determined using positron emission tomography (PET) with [18F]-2-fluoro-2-deoxy-d-glucose (18F-FDG-PET) was examined in a cohort of 237 non-demented, community-dwelling older adults aged 60–89 years (M ± SD = 73.76 ± 6.73). Higher neuroticism and lower scores on extraversion and conscientiousness were significantly associated with decreased glucose metabolism in brain regions typically affected by AD neuropathological processes, including the hippocampus and entorhinal cortex. Furthermore, while there were significant differences between apolipoprotein E (APOE) ε4 allele carriers and non-carriers on 18F-FDG-PET results in the neocortex and other brain regions (p < 0.05), there was no significant difference between carriers and non-carriers on personality factors and no significant interactions were found between APOE ε4 carriage and personality factors on brain glucose metabolism. In conclusion, we found significant relationships between personality factors and glucose metabolism in neural regions more susceptible to AD neuropathology in older adults without clinically significant cognitive impairment. These findings support the need for longitudinal research into the potential mechanisms underlying the relationship between personality and dementia risk, including measurement of change in other AD biomarkers (amyloid and tau imaging) and how they correspond to change in personality factors. Future research is also warranted to determine whether timely psychological interventions aimed at personality facets (specific aspects or characteristics of personality factors) can affect imaging or other biomarkers of AD resulting in delay or ideally preventing the onset of the cognitive impairment.
Bibliographical noteFunding Information:
The WA Memory Study (WAMS) was supported by the National Health and Medical Research Council of Australia (Grant Number: 324100 awarded to RNM), an Early Career Researcher Grant from Edith Cowan University (HRS; G1001512-2014), the Australian Alzheimer’s Research Foundation Inc., and the McCusker Charitable Foundation. The KARVIAH Study was supported by the Australian Alzheimer’s Research Foundation and the Foundation for Aged Care, Anglicare, Sydney, Australia. The authors would like to thank the WAMS and KARVIAH Study participants and research assistants and volunteers, without whose contribution this research would not be possible.
- 18F-FDG PET
- Alzheimer’s disease
- Brain ageing
- Cerebral glucose metabolism
- Five-factor model