Research Paper Volume 15, Issue 5 pp 1591—1602

The disturbance of thyroid-associated hormone and its receptors in brain and blood circulation existed in the early stage of mouse model of Alzheimer’s disease

Bingxiu Ren1, , Jinxin Ma2, , Min Tao1, , Gongwei Jing1, , Sheng Han1, , Chengyi Zhou1, , Xin Wang1, , Jiaoya Wang1, ,

  • 1 Department of Nuclear Medicine, The Third Affiliated Hospital of Zunyi Medical University (The First People’s Hospital of Zunyi), Zunyi, Guizhou 563000, China
  • 2 Department of Hospital Infection Management, The Third Affiliated Hospital of Zunyi Medical University (The First People’s Hospital of Zunyi), Zunyi, Guizhou 563000, China

Received: August 30, 2022       Accepted: February 20, 2023       Published: March 7, 2023
How to Cite

Copyright: © 2023 Ren et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Background: Studies showed that thyroid function plays an important role in the pathology of Alzheimer’s disease (AD). However, changes in brain thyroid hormone and related receptors in the early stage of AD were rarely reported. The aim of this study was to explore the relationship between the early stage of AD and local thyroid hormone and its receptors in the brain.

Methods: The animal model was established by stereotactic injection of okadaic acid (OA) into hippocampal region for the experiment, and 0.9% NS for the control. Blood sample from each mouse was collected and then the mice were sacrificed and the brain tissue was collected for detecting free triiodothyronine (FT3), free thyroid hormone (FT4), and thyroid-stimulating hormone (TSH), thyrotropin-releasing hormone (TRH) and phosphorylated tau, amyloid-β (Aβ) and thyroid hormone receptors (THRs) in the hippocampus of the mice were detected as well.

Results: Enzyme-linked immunosorbent assay showed that compared with the control, FT3, FT4, TSH and TRH in brain were significantly increased in the experimental group; in the serum, FT4, TSH and TRH were increased, while FT3 had no change; western blot analysis indicated that the expression of THR α and β in the hippocampus of the experimental group was significantly higher than that of the control.

Conclusion: Based on the results of this study, a mouse AD model can be established successfully by injecting a small dose of OA into the hippocampus. We speculate that early AD brain and circulating thyroid dysfunction may be an early local and systemic stress repair response.


AD: Alzheimer’s disease; OA: okadaic acid; NS: normal saline; FT3: free triiodothyronine; FT4: free thyroid hormone; TSH: thyroid-stimulating hormone; TRH: thyrotropin-releasing hormone; THR: thyroid hormone receptor; Elisa: Enzyme-linked immunosorbent Assay; Aβ: amyloid-β; P-Tau: phosphorylated Tau; TH: thyroid hormone; T3: 3,3′,5-triiodothyronine; T4: thyroxine; PCR: polymerase chain reaction; RT-PCR: real time polymerase chain reaction; Q-PCR: quantitative polymerase chain reaction; PP2A: Protein phosphatase 2A.