Anxiety correlates with cortical surface area in subjective cognitive decline: APOE ε4 carriers versus APOE ε4 non-carriers

Abstract

Background Subjective cognitive decline (SCD) is characterized by self-reported cognitive deficits without measurable cognitive impairment. It has been suggested that individuals with SCD exhibited brain structural alterations in widespread cortical thinning or gray matter loss in the medial temporal and frontotemporal regions. Apolipoprotein E ( APOE ) ε4 allele is thought to be a genetic marker associated with risk of SCD. Neuropsychiatric symptoms may provide insight in detecting higher-risk elders for early Alzheimer’s disease as well. Therefore, we aim to explore the characteristics of brain morphology in SCD and to determine whether it is influenced by APOE ε4 as well as neuropsychiatric symptoms in SCD. Methods A total of 138 cognitively normal older individuals from the SILCODE cohort underwent a clinical interview, neuropsychological assessments, a blood test, and MRI. A two-sample t -test was used to examine the cortex volume and bilateral cortical surface area alterations between SCD ( n = 65) and controls ( n = 73). A general linear model analysis was used to test for both main and interaction effects of clinical phenotype (SCD vs. controls) and APOE on global and regional cortex volume and bilateral cortical surface area and thickness. A multiple linear regression analysis was conducted to determine the effects of the APOE genotype on the relationships between morphometric features and neuropsychiatric symptoms in SCD. Results Compared with controls, individuals with SCD showed decreased total cortical volumes and cortical surface area. SCD APOE ε4 carriers showed additive reduction in the right cortical surface area. The evaluation scores of anxiety symptoms were negatively associated with the right cortical surface area in SCD APOE 4 non-carriers. Conclusions Individuals with SCD had an altered cortical surface area, and APOE genotype and anxiety symptoms are modified factors on the cortical surface area decrease in SCD. Trial registration ClinicalTrials.gov (Identifier: NCT03370744 ). Registered 15 March 2017. Electronic supplementary material The online version of this article (10.1186/s13195-019-0505-0) contains supplementary material, which is available to authorized users.

Neuroimaging advances regarding subjective cognitive decline in preclinical Alzheimer’s disease

“…The heterogeneity of SCD may be one of the causes of the inconsistent results, as evidence has suggested that patients with clinically defined SCD who present with smaller brain volumes have a higher risk of developing dementia than community-recruited subjects with SCD [ 23 ]. When combined with genetic risk factors, SCD subjects who are ApoE ɛ4 carriers showed more severe atrophy in the left hippocampus [ 84 ] and an additive reduction in the right cortical surface area [ 85 ] than noncarriers; this outcome is consistent with the results from longitudinal studies [ 86 ]. Furthermore, some studies have investigated the volumetric differences in subcortical regions, including the cholinergic basal forebrain nuclei and the hippocampal subfield, between individuals with SCD and HCs.…”

“… Sanchez-Benavid et al, (2018) [ 72 ] 1 binary question and SCD-Q questionnaire T1 MRI Cross-sectional NC: n = 2098 (55.41 ± 6.62) SCD-: n = 319 (55.62 ± 6.22) SCD+: n = 253 (59.10 ± 7.12) SCD+ subjects showed lower gray matter volumes. Sun et al, (2019) [ 85 ] Memory clinic consultation for < 5 y SCD T1 MRI Cross-sectional NC: n = 73 (64.55 ± 5.52) SCD: n = 65 (65.85 ± 4.85) Decreased total cortical volumes and cortical surface area in SCD. SCD ApoE ɛ4 carriers showed additive reduction in the right cortical surface area.…”

Associations Between Cerebral Morphology and Objective Memory Performance in Patients With Subjective Cognitive Decline

“…Surrounding areas including the parahippocampal gyrus are considered sites of very early formation of neuro brillary tangles in AD including early volume loss. our results have some differences from previous reports [13,44]: we did not nd signi cant cortical thickness differences between controls and SCD, which may be related to a small sample size. In addition, other factors might have also contributed to discrepant ndings between our study, e.g., the way of recruitment may in uence the results within a speci c sample.…”

Mapping the Interactive Effects of ApoE Gene Polymorphism on Caudate Functional Connectivity in Mild Cognitive Impairment Associated With Parkinson’s Disease

“…Compared to MCI in Alzheimer's disease (AD), PD-MCI frequently includes an increased severity of executive and visuospatial deficits and a decreased severity of memory impairment (Aarsland, 2016;Jellinger and Korczyn, 2018). Moreover, considering that ApoE is a well-recognized susceptibility gene for AD (Sun Y. et al, 2019), it is still far from clear whether the effects of this gene are different in PD patients.…”