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From the Departments of Neurological Sciences (Drs. Bulgakova, Leurgans, Bennett, Fleischman, and deToledo-Morrell, T.R. Stoub), Diagnostic Radiology and Nuclear Medicine (Dr. Turner), Psychology (Dr. deToledo-Morrell), and Preventive Medicine (Dr. Leurgans) and Rush Alzheimer’s Disease Center (Drs. Bennett and Fleischman), Rush University Medical Center, Chicago, IL.
Address correspondence and reprint requests to Dr. L. deToledo-Morrell, Department of Neurologic Sciences, Rush University, 1653 W. Congress Pkwy., Chicago, IL 60612; e-mail: ldetoled{at}rush.edu
Objective: To determine if baseline entorhinal and hippocampal volumes and their rate of atrophy could predict the risk of incident Alzheimer disease (AD).
Methods: The authors used proportional odds models to assess the relationship between entorhinal and hippocampal size and risk of incident AD among 58 nondemented elderly people. All participants were followed with annual clinical evaluations and structural MRI scans for up to 5 years (baseline and 5 years of follow-up). At baseline, 23 of 58 participants received a diagnosis of amnestic mild cognitive impairment (MCI) and 35 of 58 were healthy control subjects with no cognitive impairment. Structural MRI scans were acquired with a T1-weighted three-dimensional spoiled gradient-recalled echo pulse sequence in a 1.5 T scanner. Entorhinal and hippocampal volumes were derived from 1.6-mm gapless coronal images reformatted to be perpendicular to the long axis of the hippocampus and were normalized by dividing with intracranial volume.
Results: Fourteen of 58 nondemented participants developed AD during the follow-up period. Initial diagnosis of MCI was a significant predictor of incident AD. In addition, both baseline entorhinal volume and its slope of decline were independent predictors of incident AD, but initial hippocampal size and its rate of decline were not, after controlling for entorhinal volume.
Conclusion: In nondemented individuals, entorhinal cortex atrophy is associated with risk of Alzheimer disease.
Supported by grants P01 AG09466, P30 AG10161, and R01 AG17917 from the National Institute on Aging, NIH. T.R.S. received support from a predoctoral training grant (T32 AG00269) from the National Institute on Aging.
Dr. Bulgakova’s current address is Division of Neurobiology, Barrow Neurological Institute, Phoenix, AZ.
Received July 7, 2004. Accepted in final form January 7, 2005.
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