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Genes
Par Shuting Zhong, Guanfeng Xie et Zhaohui Zhang.
Contenu en anglais
Thyroid disorders and Alzheimer’s disease (AD) have been linked epidemiologically, but whether AD brain tissue and thyroid tissue affected by Hashimoto’s thyroiditis (HT) share molecular features remains unclear.
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Differential expression was estimated in AD (GSE122063) and HT (GSE138198) discovery cohorts using limma, with donor-level blocking and adjustment for age, sex and post-mortem interval where available. Shared genes were tested against chance within the genes measured in both cohorts, separately for each direction of change; characterized by enrichment analysis; related to marker-based cell-state scores; and evaluated in two AD cohorts, three thyroid cohorts including one with concurrently collected normal thyroid (GSE165724), and a single-nucleus AD dataset (GSE138852).
The discovery analyses identified 3593 AD- and 3806 HT-associated genes. The overlap was direction-specific: genes upregulated in both diseases exceeded chance (117 vs. 83.2 expected; p = 8.9 × 10−5), whereas the other direction combinations did not. Co-upregulated genes were enriched for MHC class II antigen presentation (FDR = 0.004), complement (FDR = 0.002), microglial activation (FDR = 0.017) and T-cell activation (FDR = 1.7 × 10−4), and recurred in two independent thyroid datasets and the within-study LT+ versus LT− comparison, with less consistent, region-dependent recurrence in AD cohorts. This shared component tracked immune cell-state signals—glial/myeloid activation in AD and lymphocytic infiltration in HT. Fourteen co-upregulated genes, including ITGAX, CD22 and BST2, met prespecified recurrence and detectability criteria.
AD brain tissue and thyroid tissue affected by HT exhibit a co-upregulated immune and antigen-presentation transcriptional program that reflects immune activation in both tissues. These overlapping features are associative and do not establish a causal relationship between AD and HT.
Publié dans Genes. Le résumé est reproduit tel qu’il a été publié et reste l’œuvre de ses auteurs ; lisez l’article complet à la source.
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