I. Horbachevsky Ternopil National Medical University, Ukraine.
HSEEU "Bukovinian State Medical University", Chernivtsi, Ukraine.
Endocr Regul. 2021 Dec 7;55(4):193-203. doi: 10.2478/enr-2021-0021.
Brain-derived neurotrophic factor (BDNF) is identified as an important growth factor involved in learning and memory. Patients with Hashimoto's thyroiditis can suffer from cognitive dysfunction, whereas BDNF is directly regulated by thyroid hormones. It seems reasonable to propose that changes in BDNF expression underlie some of the persistent neurological impairments associated with hypothyroidism. The study involved a total of 153 patients with various forms of thyroid pathology. BDNF levels in the sera of the patients and healthy individuals were quantified using enzyme-linked immunosorbent assay with highly sensitive Human BDNF ELISA Kit. Genotyping of the BDNF (rs6265) gene polymorphism using TaqMan probes and TaqMan Genotyping Master Mix (4371355) on CFX96™Real-Time PCR Detection System. Polymerase chain reaction (PCR) for TaqMan genotyping was carried out according to the kit instructions. Distribution rs6265 variants in the patients depending on the different types of thyroid pathology showed no significant difference in the relative frequency of BDNF polymorphic variants. Presence of hypothyroidism, regardless of its cause (autoimmune or postoperative), there was a decrease in the serum BDNF levels in all genotypes carriers compared with the control group. The analysis of the correlation between BDNF levels and the levels of thyroid-stimulating hormone (TSH), thyroxine (T4), anti-thyroglobulin (anti-Tg), and anti-thyroid peroxidase (anti-TPO) antibodies showed a significant inverse relationship between BDNF and TSH levels (p<0.001), a direct correlation between BDNF and T4 levels in the blood (p<0.001), and a weak direct relationship between anti-Tg and BDNF levels (p=0.0157). The C allele presence is protective and associates with the lowest chances for reduced serum BDNF levels in thyroid pathology patients in the West-Ukrainian population. However, the T-allele increases the risk of low BDNF levels almost 10 times in observed subjects.
脑源性神经营养因子（BDNF）被确定为参与学习和记忆的重要生长因子。桥本甲状腺炎患者可出现认知功能障碍，而 BDNF 直接受甲状腺激素调节。因此，可以合理地提出，BDNF 表达的变化是甲状腺功能减退症相关持续神经损伤的部分原因。该研究共纳入了 153 名患有各种甲状腺疾病的患者。采用高度敏感的人 BDNF ELISA 试剂盒通过酶联免疫吸附试验（ELISA）定量检测患者和健康个体血清中的 BDNF 水平。采用 TaqMan 探针和 TaqMan 基因分型 MasterMix（4371355）在 CFX96™实时 PCR 检测系统上对 BDNF（rs6265）基因多态性进行基因分型。根据试剂盒说明进行 TaqMan 基因分型的聚合酶链反应（PCR）。根据试剂盒说明进行 TaqMan 基因分型的聚合酶链反应（PCR）。
根据不同类型的甲状腺病理学，BDNF rs6265 变体在患者中的分布没有显示 BDNF 多态变体的相对频率存在显著差异。存在甲状腺功能减退症，无论其病因（自身免疫性或术后）如何，与对照组相比，所有基因型携带者的血清 BDNF 水平均降低。BDNF 水平与促甲状腺激素（TSH）、甲状腺素（T4）、抗甲状腺球蛋白（anti-Tg）和抗甲状腺过氧化物酶（anti-TPO）抗体水平之间的相关性分析显示，BDNF 与 TSH 水平之间存在显著的负相关关系（p<0.001），BDNF 与血液中的 T4 水平之间存在直接的正相关关系（p<0.001），anti-Tg 和 BDNF 水平之间存在微弱的直接关系（p=0.0157）。C 等位基因的存在是保护性的，与西乌克兰人群中甲状腺疾病患者血清 BDNF 水平降低的几率最低相关。然而，T 等位基因使观察到的对象中 BDNF 水平降低的风险增加了近 10 倍。
