Affiliations: [a] Dementia Collaborative Research Centre, School of Psychiatry, UNSW Medicine, University of New South Wales, Sydney, Australia | [b] Centre for Health Brain Ageing, School of Psychiatry, UNSW Medicine, University of New South Wales, Sydney, Australia | [c] Neuropsychiatric Institute, Prince of Wales Hospital, Randwick, NSW, Australia | [d] Academic Department for Old Age Psychiatry, Prince of Wales Hospital, Sydney, Australia | [e] Department of Developmental Disability Neuropsychiatry, School of Psychiatry, University of New South Wales, Sydney, Australia
Abstract: Alcohol consumption is a potentially modifiable risk factor for dementia, but the literature is not completely consistent. This inconsistency may be partly due to an interaction with the apolipoprotein E (APOE) genotype, an established risk factor for Alzheimer’s dementia. The aim of this study was to examine whether alcohol consumption is associated with incident dementia or decline in specific cognitive domains over 4 years, and if this effect is modified by APOE ɛ4 status. Non-demented community dwelling older adults (70-90 years) from an ongoing longitudinal study were assessed for cognitive impairment in attention/processing speed, language, executive function, visuospatial ability, and memory. Incident dementia was diagnosed according to DSM-IV criteria. Compared to those who did not drink in the previous 12 months, neither low consumption (HR 0.64 95% CI 0.3-1.4) or risky consumption (HR 0.58 95% CI 0.2-1.5) was associated with incident dementia. Carriers of the APOE ɛ4 allele were more likely to develop dementia, but there was no significant interaction with alcohol consumption.
