Racine, Annie M.Fong, TamaraTravison, ThomasJones, Richard N.Gou, YunVasunilashorn, SarinnaphaMarcantonio, EdwardAlsop, DavidInouye, SharonDickerson, Bradford2021-08-302017-11Racine, Annie M., Tamara G. Fong, Thomas G. Travison, Richard N. Jones, Yun Gou, Sarinnapha M. Vasunilashorn, Edward R. Marcantonio, David C. Alsop, Sharon K. Inouye, and Bradford C. Dickerson. “Alzheimer’s-Related Cortical Atrophy Is Associated with Postoperative Delirium Severity in Persons without Dementia.” Neurobiology of Aging 59 (November 2017): 55–63. https://doi.org/10.1016/j.neurobiolaging.2017.07.010.0197-45801558-1497https://nrs.harvard.edu/URN-3:HUL.INSTREPOS:37369184Patients with dementia due to Alzheimer’s disease (AD) have increased risk of developing delirium. This study investigated the relationship between a magnetic resonance imaging (MRI)-derived biomarker associated with preclinical AD and postoperative delirium. Participants were older adults (≥70 years) without dementia who underwent preoperative MRI and elective surgery. Delirium incidence and severity were evaluated daily during hospitalization. Cortical thickness was averaged across a published set of a priori brain regions to derive a measure known as the “AD signature.” Logistic and linear regression was used, respectively, to test whether the AD signature was associated with delirium incidence in the entire sample (N=145) or with the severity of delirium among those who developed delirium (N=32). Thinner cortex in the AD signature did not predict incidence of delirium (odds ratio=1.15, p=.38), but was associated with greater delirium severity among those who developed delirium (b=−1.2, p=.014). These results suggest that thinner cortices, perhaps reflecting underlying neurodegeneration due to preclinical AD, may serve as a vulnerability factor that increases severity once delirium occurs.en-USJournal Article2021-08-3010.1016/j.neurobiolaging.2017.07.010