Objective: This study examined the volume of choroid plexus across AD without delusion (AD-D), AD with paranoid delusion (AD+PD), and AD with misidentification delusion (AD+MD). Methods: This is a hospital based cross-sectional study of patients with AD. The main outcome measure is the volume of choroid plexus that were measured as regions of interest with magnetic resonance imaging and the FreeSurfer analysis at baseline. Analysis of covariance (ANCOVA) was conducted to compare the differences on the volume of choroid plexus across AD-D, AD+PD, and AD+MD after controlling demographics. Results: There was no volume difference in the both choroid plexus between AD-D and AD+D. However, the volumes of both cho-roid plexus were significantly reduced in AD+MD compared to AD+PD. Conclusion Our study demonstrates that AD+MD has significantly reduced volumes of choroid plexus compared to AD+PD. These findings suggest that AD+MD and AD+PD may have different pathophysiological mechanisms related to neuroimmune re-sponses in the choroid plexus.

Objective: Although previous studies have shown association between anterior corpus callosum (ACC) and various psychotic disorder, the effect of ACC on development on psychotic symptoms in Alzheimer’s disease (AD) is still unclear. The purpose of this study is to investigate the association of ACC with the development of psychosis in patients with AD. Methods: This is a hospital based cross-sectional study of 241 AD patients. The main outcome measure is the volume of ACC that were measured as regions of interest with magnetic resonance imaging and the FreeSurfer analysis at baseline. Analysis of covariance and Logistic regression analysis conducted to assess the association between the volume of ACC and the presence of psychosis in AD, adjusting for age, education, Clinical Dementia Rating-Sum of Boxes, and total intracranial volume. Results: We found that the volume of ACC is significantly reduced in AD with psychosis (AD+P) compared to AD without psychosis (AD-P) (774.27±142.96 vs. 833.09±142.04, p=0.005). The volume of ACC associated with the presence of psychosis in AD (odds ratio=0.995; 95% confidence interval=0.993-0.997; p=0.006). Conclusion We have found that reduced volume of ACC in AD+P, suggesting that ACC might play an important role in the underlying pathogenesis of development of psychotic symptoms in AD.

Objective: The purpose of this study is to investigate the association of the apolipoprotein E (APOE) e4 genotype with cognition, brain volume, glucose metabolism, and amyloid deposition in patients with Alzheimer disease (AD). Methods: This is cross-sectional study of 69 subjects with AD. All subjects were divided into carriers and non-carriers of the e4 allele. Forty APOE e4 carriers and 29 APOE e4 non-carriers underwent neuropsychological, structural magnetic resonance imaging, [18F]fluorodeoxyglucose positron emission tomography scans (PET) and [18F]florbetaben amyloid PET. Analysis of co-variance was conducted to compare the differences on cognition, brain volume, glucose metabolism and amyloid deposition between APOE e4 carriers and non-carriers after controlling demographics. Results: APOE e4 carriers had 50% lower scores of Seoul Verbal Learning Test (delayed recall) compared to non-carriers (0.88±1.65 vs. 1.76±1.75, p<0.05). However, APOE e4 carriers performed better on other cognitive tests than non-carriers (Korean version of Boston Naming Test [11.04±2.55 vs. 9.66±2.82, p<0.05], Rey Complex Figure Test [25.73±8.56 vs. 20.15±10.82, p<0.05], and Stroop test [color response] [48.28±26.33 vs. 31.56±27.03, p<0.05]). APOE e4 carriers had slightly smaller hippocampal volume than non-carriers (3.09±0.38 vs. 3.32±0.38, p<0.05), but greater total brain cortical thickness (1.45±1.55 vs. 1.37±1.24, p<0.05). Amyloid deposition did not differ significantly between APOE e4 carriers and non-carriers, and no signifi-cant difference in glucose metabolism was found between groups. Conclusion We found that APOE e4 genotype is associated with cognition, brain volume in AD, suggesting that APOE e4 genotype could play an important role in the underlying pathogenesis of AD.

Objective: Apolipoprotein E (APOE) genotype is associated with risk of Alzheimer’s disease (AD), but the association ofAPOE ε4 allele with longitudinal medial temporal lobe atrophy (MTA) has been controversial. This study aims to evaluate the effect of APOE genotype on longitudinal MTA over a 2-year period in cognitively impaired patients with amyloid deposition. Methods: This retrospective longitudinal study included 65 cognitively impaired subjects with amyloid deposition (subjective memory impairment, mild cognitive impairment, and mild AD). Participants were divided into carriers (n=27) and non-carriers (n=38) of the ε4 allele. The main outcome is longitudinal reduction of medial temporal lobe (hippocampus, entorhinal cortex, and parahippocampal gyrus) over 2 years. Analysis of covariance was conducted to compare the differences in longitudinal MTA between groups, controlling for covariates. Results: At baseline, hippocampal volume was 4.6% smaller (6.38±1.13 vs. 6.69±0.83, p=0.026) and entorhinal thickness was6.4% thinner (3.51±0.57 vs. 3.75±0.52, p=0.033) in APOE ε4 carriers than non-carriers. Furthermore, APOE ε4 carriers had significantly 72% greater longitudinal hippocampal atrophy compared to non-carriers (-0.43±0.30 vs. -0.25±0.31, p=0.041). Conclusion Our findings of baseline or longitudinal MTA in APOE ε4 carriers suggest that APOE ε4 genotype may contrib-ute to underlying pathophysiology of medial temporal lobe in AD.