Reduced Thickness of the Anterior Cingulate Cortex as a Predictor of Amnestic-Mild Cognitive Impairment Conversion to Alzheimer’s Disease with Psychosis
Affiliations: [a]
Department of Psychiatry, Pusan National University School of Medicine, Busan, Republic of Korea
| [b]
Biomedical Research Institute, Pusan National University Hospital, Busan, Republic of Korea
| [c]
Department of Radiology, Pusan National University School of Medicine, Busan, Republic of Korea
| [d]
Department of Nuclear Medicine, Pusan National University School of Medicine, Busan, Republic of Korea
| [e]
Department of Pathology, Pusan National University School of Medicine, Busan, Republic of Korea
| [f]
Department of Psychiatry, Pusan National University School of Medicine, Yangsan, Republic of Korea
Correspondence:
[*]
Correspondence to: Dr. Young-Min Lee, MD, PhD, Department of Psychiatry, School of Medicine, Pusan National University, 305 Gudeok-Ro, Seo-Gu, Busan 602-739, Republic of Korea. Tel.: +82 51 240 7301; Fax: +82 51 248 3648; E-mail: psyleekr@naver.com.
Abstract: Background:A long-term follow-up study in patients with amnestic mild cognitive impairment (aMCI) is needed to elucidate the association between regional brain volume and psychopathological mechanisms of Alzheimer’s disease with psychosis (AD + P). Objective:The purpose of this study was to investigate the effect of the thickness of the angular cingulate cortex (ACC) on the risk of AD + P conversion in patients with aMCI. Methods:This was a hospital-based prospective longitudinal study including 174 patients with aMCI. The main outcome measure was time-to-progression from aMCI to AD + P. Subregions of the ACC (rostral ACC, rACC; caudal ACC, cACC) and hippocampus (HC) were measured as regions of interest with magnetic resonance imaging and the Freesurfer analysis at baseline. Survival analysis with time to incident AD + P as an event variable was calculated with Cox proportional hazards models using the subregions of the ACC and HC as a continuous variable. Results:Cox proportional hazard analyses showed that the risk of AD + P was associated with sub-regional ACC thickness but not HC volume: reduced cortical thickness of the left cACC (HR [95%CI], 0.224 [0.087–0.575], p = 0.002), right cACC (HR [95%CI], 0.318 [0.132–0.768], p = 0.011). This association of the cACC with the risk of AD also remained significant when adjusted for HC volume. Conclusion:We found that reduced cortical thickness of the cACC is a predictor of aMCI conversion to AD + P, independent of HC, suggesting that the ACC plays a vital role in the underlying pathogenesis of AD + P.
