Associations of thyroid hormone serum levels with in-vivo Alzheimer's disease pathologies

The present study investigated the relationships between thyroid hormone serum levels or thyroid-stimulating hormone (TSH) and two Alzheimer's disease (AD)-specific biomarkers, cerebral amyloid beta (Aβ) burden and glucose metabolism, in AD-signature brain regions in cognitively normal (CN) mid...

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Published inAlzheimer's research & therapy Vol. 9; no. 1; p. 64
Main Authors Choi, Hyo Jung, Byun, Min Soo, Yi, Dahyun, Sohn, Bo Kyung, Lee, Jun Ho, Lee, Jun-Young, Kim, Yu Kyung, Lee, Dong Young
Format Journal Article
LanguageEnglish
Published England BioMed Central 17.08.2017
BMC
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Summary:The present study investigated the relationships between thyroid hormone serum levels or thyroid-stimulating hormone (TSH) and two Alzheimer's disease (AD)-specific biomarkers, cerebral amyloid beta (Aβ) burden and glucose metabolism, in AD-signature brain regions in cognitively normal (CN) middle-aged and older individuals. This study assessed 148 CN individuals who received comprehensive clinical and neuropsychological assessments that included C-Pittsburgh Compound B (PiB)-positron emission tomography (PET) scans, F-deoxyglucose (FDG)-PET scans, and the quantification of serum triiodothyronine (T3), free T3, free thyroxine (fT4), and TSH levels. All participants were clinically euthyroid. Independent negative associations were found between serum fT4 levels and global cerebral Aβ deposition after controlling for the effects of age, gender, and the apolipoprotein E ε4 (APOEε4) genotype. Although serum TSH levels were not associated with global cerebral Aβ deposition, they had a significant negative association with glucose metabolism in the precuneus/posterior cingulate cortex after controlling for age, gender, and the APOEε4 genotype. No other thyroid hormones exhibited relationships with either brain Aβ burden or glucose metabolism. Even in a clinical euthyroid state, low serum fT4 and high serum TSH levels appear to be differentially associated with AD-specific brain changes.
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ISSN:1758-9193
1758-9193
DOI:10.1186/s13195-017-0291-5