Cortical thinning in temporal pole, a core region in Alzheimer's disease, in non-demented, middle-aged APOE-e4 and PICALM-AA/AG carriers

Abstract

The symptoms of Alzheimers disease (AD) are caused by neurodegeneration and atrophy in particular brain regions, especially in the temporal cortex. However, the influence of genetic risk on cortical thickness in non-demented individuals prior to disease onset remains unclear. This study aimed to explore the relationship between two AD risk genes (APOE/PICALM) and cortical thickness in selected regions of interest (ROIs) in non-demented, middle-aged individuals. Sixty-nine (N = 69) participants (34 females, 35 males; age: 55.45{+/-}3.19) underwent magnetic resonance imaging (MRI). They were divided into three groups based on their AD risk. Cortical thickness was analyzed using CAT12 software (surface-based morphometry with the Destrieux atlas) based on T1-weighted MR images in five ROIs referred as "the cortical signature of AD" in previous studies. APOE-{varepsilon}4 with PICALM-AA/AG carriers (A+P-) are characterized by a thinner cortex in the right temporal pole compared to non-carriers, controlling for sex. No other differences in cortical thickness were found in the selected ROIs. The direction of the findings aligns with existing literature reporting cortical thinning in amyloid-positive individuals, as well as in patients with mild cognitive impairment and Alzheimers disease when compared to control groups.