You could be reading the full-text of this article now if you...

If you have access to this article through your institution,
you can view this article in

Cardiovascular Risk Factors Cause Cortical Thinning in Cognitively Impaired Patients: Relationships Among Cardiovascular Risk Factors, White Matter Hyperintensities, and Cortical Atrophy

Seo, Sang Won MD, PhD*; Lee, Jong-Min PhD; Im, Kiho PhD; Park, Jun-Sung MS; Kim, Sook-Hui MD§; Kim, Sung Tae MD, PhD; Ahn, Joong Hyun MS; Kim, Min-Jeong MD#; Kim, Geon Ha MD*; Kim, Jong Hun MD**; Roh, Jee Hoon MD††; Cheong, Hae-Kwan MD, PhD‡‡; Na, Duk L. MD*

Alzheimer Disease & Associated Disorders:
doi: 10.1097/WAD.0b013e31822e0831
Original Articles
Abstract

Cardiovascular risk factors are associated with cognitive impairments. However, the effects of cardiovascular risk factors on the topography of cortical thinning have not yet been studied in patients with mild cognitive impairment (MCI) or dementia. Thus, we aimed to evaluate the topography of cortical thinning related to cardiovascular risk factors and the relationships among cardiovascular risk factors, white matter hyperintensities (WMH), and cortical atrophy. Participants included 226 patients with Alzheimer disease or subcortical vascular dementia and 135 patients with amnestic MCI or subcortical vascular MCI. We automatically measured the volume of WMH and cortical thickness. Hypertension was associated with cortical thinning in the frontal and perisylvian regions, and cortical thinning related to diabetes mellitus (DM) occurred in the frontal region. In path analyses, hypertension accounted for 0.04 of the frontal thinning with the mediation of WMH and 0.16 without the mediation of WMH. In case of DM, it accounted for 0.02 of the frontal thinning with the mediation of WMH and 0.13 without the mediation of WMH. Hypertension and DM predominantly affected frontal thinning both with and without the mediation of WMH, where the effects without the mediation of WMH were greater than those with the mediation of WMH.

Author Information

*Department of Neurology, Sungkyunkwan University School of Medicine, Samsung Medical Center

Department of Biomedical Engineering, Hanyang University

§Department of Neurology, Konkuk University Hospital, Konkuk University School of Medicine

Department of Radiology, Sungkyunkwan University School of Medicine

Biostatistics team, Samsung Biomedical Research Institute, Samsung Medical Center

#Department of Neurology, Seoul National University Boramae Hospital

**Department of Neurology, National Health Insurance Corporation Ilsan Hospital, Goyang, Republic of Korea

‡‡Department of Social and Preventive Medicine, Sungkyunkwan University School of Medicine, Samsung Medical Center, Seoul, Korea

††Department of Neurology, Washington University School of Medicine, St Louis, MO

Division of Newborn Medicine, Children’s Hospital Boston, Harvard Medical School, MA

This study was supported by a grant from the Korean Healthcare Technology R&D Project, Ministry for Health, Welfare & Family Affairs, Republic of Korea (A050079), a Korean Science and Engineering Foundation (KOSEF) NRL Program Grant funded by the Korean government (MEST; R0A-2007-000-20068-0), and a Samsung Medical Center Clinical Research Development Program Grant (CRL-108011 & CRS 110-14-1).

The authors declare no conflict of interest.

This study was approved by the Institutional Review Board of the Samsung Medical Center.

Reprints: Duk L. Na, MD, Department of Neurology, Sungkyunkwan University, Samsung Medical Center, 50 Ilwon-dong, Kangnam-ku, Seoul 135-710, Korea (e-mail: dukna@skku.edu).

Received February 23, 2011

Accepted May 31, 2011

© 2012 Lippincott Williams & Wilkins, Inc.