Affiliations: [a] Harvard-MIT Division of Health Sciences and Technology, Cambridge, MA, USA
| [b]
Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA, USA
| [c] Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA
| [d] Computer Science and Artificial Intelligence Laboratory (CSAIL), Massachusetts Institute of Technology (MIT), Cambridge, MA, USA
| [e]
Neuroimaging Research for Veterans (NeRVe) Center, VA Boston Healthcare System, Boston, MA, USA
Correspondence:
[*]
Correspondence to: Emily R. Lindemer, BSc, Massachusetts General Hospital Athinoula A. Martinos Center for Biomedical Imaging, Bldg. 149 13th St., CNY 2301, Charlestown, MA 02129, USA. Tel.: +1 617 726 3197; Fax: +1 617 726 7422; E-mail: [email protected].
Note: [1] Data used in preparation of this article were obtained from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database (http://adni.loni.usc.edu). As such, the investigators within the ADNI contributed to the design and implementation of ADNI and/or provided data but did not participate in analysis or writing of this report. A complete listing of ADNI investigators can be found at: http://adni.loni.usc.edu/wp-content/uploads/how_to_apply/ADNI_Acknowledgement_List.pdf..
Abstract: Background: White matter signal abnormalities (WMSA) (also known as ‘hyperintensities’) on MRI are commonly seen in normal aging and increases have been noted in Alzheimer’s disease (AD), but whether there is a spatial specificity to these increases is unknown. Objective: To discern whether or not there is a spatial pattern of WMSA in the brains of individuals with AD that differs from those who exhibit cognitively healthy aging. Method: Structural MRI data from the Alzheimer’s Disease Neuroimaging Initiative public database were used to quantify WMSA in 35 regions of interest (ROIs). Regional measures were compared between cognitively healthy older controls (OC; n = 107) and individuals with a clinical diagnosis of AD (n = 127). Regional WMSA volume was also assessed in individuals with mild cognitive impairment (MCI; n = 74) who were 6, 12, and 24 months away from AD conversion. Results: WMSA volume was significantly greater in AD compared to OC in 24 out of 35 ROIs after controlling for age, and nine were significantly higher after normalizing for total WMSA. Regions with greater WMSA volume in AD included rostral frontal, inferior temporal, and inferior parietal WM. In MCI, frontal and temporal regions demonstrated significantly greater WMSA volume with decreasing time-to-AD-conversion. Discussion: Individuals with AD have greater regional volume of WMSA compared to OC regardless of age or total WMSA volume. Accumulation of regional WMSA is linked to time to AD conversion in individuals with MCI. These findings indicate WMSA is an important pathological component of AD development.
Keywords: Aging, Alzheimer’s disease, cerebrovascular, hyperintensities, magnetic resonance imaging, mild cognitive impairment, white matter
