| First Author | Li Y | Year | 2024 |
| Journal | Biochem Biophys Res Commun | Volume | 704 |
| Pages | 149723 | PubMed ID | 38430698 |
| Mgi Jnum | J:361028 | Mgi Id | MGI:7615817 |
| Doi | 10.1016/j.bbrc.2024.149723 | Citation | Li Y, et al. (2024) TSHR signaling promotes hippocampal dependent memory formation through modulating Wnt5a/beta-catenin mediated neurogenesis. Biochem Biophys Res Commun 704:149723 |
| abstractText | Subclinical hyperthyroidism is defined biochemically as a low or undetectable thyroid-stimulating hormone (TSH) with normal thyroid hormone levels. Low TSHR signaling is considered to associate with cognitive impairment. However, the underlying molecular mechanism by which TSHR signaling modulates memory is poorly understood. In this study, we found that Tshr-deficient in the hippocampal neurons impairs the learning and memory abilities of mice, accompanying by a decline in the number of newborn neurons. Notably, Tshr ablation in the hippocampus decreases the expression of Wnt5a, thereby inactivating the beta-catenin signaling pathway to reduce the neurogenesis. Conversely, activating of the Wnt/beta-catenin pathway by the agonist SKL2001 results in an increase in hippocampal neurogenesis, resulting in the amelioration in the deficits of memory caused by Tshr deletion. Understanding how TSHR signaling in the hippocampus regulates memory provides insights into subclinical hyperthyroidism affecting cognitive function and will suggest ways to rationally design interventions for neurocognitive disorders. |
