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Hypothalamic-Pituitary-Thyroid Axis in Patients With Alzheimer Disease (AD)
  1. Li Yong-Hong, MD*,
  2. Peng Xiao-Dong, MD,
  3. Huang Chang-Quan, MD*‡,
  4. Yang Bo, PhD*,
  5. Liu Qing-Xiu, MD
  1. From the *Key Laboratory of Biological Effect of Physical Field and Instrument of Sichuan Provincial Department of Education; Department of Electronic Engineering, Chengdu University of Information Technology, Chengdu, Sichuan, China; †Department of Oncology, The Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan, China; and ‡Department of Geriatrics, The Third Hospital of Mianyang, Sichuan, China.
  1. Yong-Hong and Xiao-Dong contributed equally to this work.
  2. Received January 31, 2012, and in revised form September 5, 2012.
  3. Accepted for publication September 21, 2012.
  4. Reprints: Huang Chang-Quan, MD, Key Laboratory of Biological Effect of Physical Field and Instrument of Sichuan Provincial Department of Education; Department of Electronic Engineering, Chengdu University of Information Technology, Chengdu, Sichuan 610225, China. E-mail: huanghanjie03{at}yahoo.com.cn.
  5. Supported by Science and Technology Graveness Project of Sichuan Province (2010FZ0061) and the Scientific Research Foundation Project of CUIT (KYTZ201021) and the Illustrious Youth Specialist Project of Sichuan Province (2012JQ0050) and the National Natural Science Foundation of China (81101898).
  6. The authors have no conflicts of interest.

Abstract

Objective We observed the function of hypothalamic-pituitary-thyroid axis in patients with Alzheimer disease (AD) using a case-control study.

Methods The case was a cohort that included 50 patients with AD. For each case subject, 1 control who was of similar age, sex, daily activities (scale of Lawton), sleep quality (Pittsburgh Sleep Quality Index), and depression (15-item Geriatrics Depression Scale) was recruited. Thyrotropin-releasing hormone (TRH), thyroid-stimulating hormone (TSH), total triiodothyronine (TT3), total tetraiodothyronine (TT4), free triiodothyronine (FT3), and free tetraiodothyronine (FT4) were detected using radioimmunity.

Results Compared with the healthy controls, the patients with AD had significantly lower levels of TRH (67.72 ± 18.44 vs 78.64 ± 14.31 pmol/L; t = 2.078; P = 0.036), TSH (3.89 ± 1.22 vs 4.31 ± 1.07 mIU/L; t = 2.331; P = 0.024), TT3 (1.44 ± 0.21 vs 1.63 ± 0.19 nmol/L; t = 3.761; P = 0.018), TT4 (119.71 ± 18.64 nmol/L vs 129.54 ± 23.17 nmol/L; t = 1.328; P = 0.044), FT3 (4.01 ± 1.27 vs 5.41 ± 0.99 pmol/L; t = 4.976; P = 0.008), and FT4 (9.84 ± 1.56 vs 12.96 ± 2.20 pmol/L; t = 5.381; P = 0.006). In the AD cases, none of the correlations between TRH and TSH, TT3, TT4, FT3, and FT4, and between TSH and TT3, TT4, FT3, FT4 was significant. However, in the healthy controls, TRH was significantly correlated with TSH (R = 0.020; P = 0.042) and FT4 (R = 0.015; P = 0.018), and TSH was significantly correlated with TT4 (R = 0.209; P = 0.017) and FT4 (R = 0.215; P = 0.009).

Conclusion Alzheimer disease was associated with abnormal function of the hypothalamic-pituitary-thyroid axis.

Key Words
  • hypothalamic-pituitary-thyroid axis
  • hormone
  • Alzheimer disease
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