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Article type: Article Commentary
Authors: Bini, Jason; *
Affiliations: Department of Radiology and Biomedical Imaging, Yale University School of Medicine, New Haven, CT, USA
Correspondence: [*] Correspondence to: Jason Bini, PhD, Yale PET Center, Yale University School of Medicine, PO Box 208, New Haven, CT 06519, USA. E-mail: jason.bini@yale.edu; ORCID: 0000-0003-4047-6575
Abstract: Excess cortisol is associated with more severe cognitive decline, Alzheimer’s disease, and related dementia phenotypes. The intracellular enzyme 11β-HSD1 regenerates active cortisol from inactive cortisone. In this current issue, high regional brain occupancy of Xanamemtrademark, determined by [11C]TARACT PET imaging of 11β-HSD1, in cognitively normal individuals and mild cognitive impartment/Alzheimer’s disease (AD) patients is presented. In the future, comprehensive kinetic modeling using arterial sampling for occupancy studies, and whole-body PET imaging of 11β-HSD1 enzyme levels, in combination with stable isotope studies of cortisol metabolism, can provide broad insight into enzyme levels and activity in AD and other relevant diseases.
Keywords: Alzheimer’s disease, cortisol, positron emission tomography, 11β-hydroxysteroid dehydrogenase type 1
DOI: 10.3233/JAD-231463
Journal: Journal of Alzheimer's Disease, vol. 99, no. 1, pp. 113-115, 2024
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