Affiliations: [a] Department of Radiology, Washington University School of Medicine, St. Louis, MO, USA | [b] Department of Neurosurgery, Washington University School of Medicine, St. Louis, MO, USA | [c] Department of Neurology, Washington University School of Medicine, St. Louis, MO, USA | [d] Department of Psychiatry, Washington University School of Medicine, St. Louis, MO, USA | [e] Departments of Radiology, Neurology, and Psychiatry, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA | [f] Departments of Biostatistics, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA
Correspondence:
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Correspondence to: Dr. Yvette I. Sheline, MD, University of Pennsylvania Perelman School of Medicine, 3535 Market Street, Philadelphia, PA 19104, USA. Tel.: +1 215 573 0082; Fax: +1 215 349 5067; E-mail: sheline@mail.med.upenn.edu.
Abstract: The earliest sites of brain atrophy in Alzheimer's disease are in the medial temporal lobe, following widespread cerebral cortical amyloid deposition. We assessed 74 cognitively normal participants with clinical measurements, amyloid-β-PET imaging, MRI, and a newly developed technique for MRI-based hippocampal subfield segmentation to determine the differential association of amyloid deposition and hippocampal subfield volume. Compared to amyloid-negative participants, amyloid-positive participants had significantly smaller hippocampal tail, presubiculum, subiculum, and total hippocampal gray matter volumes. We conclude that, prior to the development of cognitive impairment, atrophy in particular hippocampal subfields occurs preferentially with amyloid-β accumulation.
