ASSOCIATION BETWEEN APOE-epsilon(4) CARRIER STATUS AND QUALITATIVE NEUROIMAGING CHARACTERISTICS IN OLDER ADULTS WITH MILD COGNITIVE IMPAIRMENT

Background: The pathogenesis of mild cognitive impairment (MCI) is multifactorial and includes the presence of genetic variants such as the epsilon(4) allele of the apolipoprotein E gene (APOE-epsilon(4)). Association between the APOE-epsilon(4) carrier status and deleterious structural and functional changes on magnetic resonance imaging (MRI) has been previously described in individuals with Alzheimer's disease. However, the central nervous system changes may possibly develop in earlier stages of cognitive impairment, as reflected in MCI. Objective: The objective of the study was to determine the association between APOE-epsilon(4) carrier status and qualitative changes on MRI (medial temporal and parietal atrophy), as well as the detection of white matter hyperintensities (WMH) in older adults with MCI, in the memory clinic of a tertiary care hospital in Mexico City. Methods: A cross-sectional study of 72 adults aged 60 years or above who underwent an exhaustive clinical, neuroimaging, and neuropsychological evaluation. Multivariate logistic regression models were constructed to determine the association between APOE-epsilon(4) carrier status and qualitative/quantitative changes on MRI. Results: Mean age was 75.2 years (+/- 7.2) and 64% were female. Twenty-one participants were cognitively normal and 51 had MCI. Almost 56% were APOE-epsilon(4) carriers and were associated with medial-temporal atrophy according to the Scheltens scale (odds ratio [OH: 20.0, 95% confidence intervals [CI): 3.03-131.7), parietal atrophy according to the Koedam's score (OR: 6.3; 95% CI 1.03-39.53), and WMH according to the Fazekas scale (OR: 11.7, 95% CI: 1.26-108.2), even after adjusting for age, educational level, and cardiovascular risk factors. Conclusion: The APOE-epsilon(4) carrier status was associated with medial temporal and parietal atrophy, as well as WMH. Our findings support the hypothesis suggesting the contribution of this genotype to neurodegeneration and cerebral vascular pathology.