Background Adipokines are hormones secreted by adipose tissue with roles in energy homeostasis and regulation of metabolism. Their dysregulation is suggested to contribute to the increased risk of dementia seen with midlife obesity, but longitudinal studies investigating this are scarce. We determined the association between plasma levels of adiponectin, leptin, and resistin with the risk of dementia. Methods We performed a case–cohort study embedded in the prospective, population-based Rotterdam Study. Plasma levels of the adiponectin, leptin, and resistin were measured at baseline (1997–1999) in a random subcohort of 945 participants without dementia, and additionally in 177 participants, who were diagnosed with dementia during follow-up (until January 1, 2018). Results Higher levels of leptin and resistin were associated with a decreased risk of dementia (adjusted hazard ratio [95% confidence interval] per SD increase of log-transformed values: 0.85 [0.72–1.00] for leptin; 0.82 [0.71–0.95] for resistin). The association of leptin with dementia was further modified by body mass index and by APOE ε4 carrier status. Adiponectin levels were not associated with the risk of dementia. Conclusions These findings support the hypothesis that adipokines have a role in the pathophysiology of dementia. Future studies are warranted to confirm the findings and to explore the underlying mechanisms.

中文翻译：

---

脂联素、瘦素和抵抗素与痴呆症的风险

背景脂肪因子是由脂肪组织分泌的激素，在能量稳态和代谢调节中发挥作用。他们的失调被认为会导致中年肥胖导致痴呆症的风险增加，但对此进行调查的纵向研究很少。我们确定了血浆脂联素、瘦素和抵抗素水平与痴呆风险之间的关联。方法 我们在前瞻性、基于人群的鹿特丹研究中进行了病例队列研究。脂联素、瘦素和抵抗素的血浆水平在基线（1997-1999 年）测量了 945 名无痴呆症参与者的随机亚组，另外还有 177 名在随访期间被诊断出患有痴呆症的参与者（直到 2018 年 1 月 1 日） ）。结果 较高水平的瘦素和抵抗素与痴呆风险降低相关（调整后的风险比 [95% 置信区间] 每 SD 增加对数转换值：瘦素为 0.85 [0.72–1.00]；瘦素为 0.82 [0.71–0.95]抵抗素）。体重指数和 APOE ε4 携带者状态进一步改变了瘦素与痴呆的关联。脂联素水平与痴呆风险无关。结论 这些发现支持脂肪因子在痴呆的病理生理学中起作用的假设。未来的研究有必要证实这些发现并探索潜在的机制。体重指数和 APOE ε4 携带者状态进一步改变了瘦素与痴呆的关联。脂联素水平与痴呆风险无关。结论 这些发现支持脂肪因子在痴呆的病理生理学中起作用的假设。未来的研究有必要证实这些发现并探索潜在的机制。体重指数和 APOE ε4 携带者状态进一步改变了瘦素与痴呆的关联。脂联素水平与痴呆风险无关。结论 这些发现支持脂肪因子在痴呆的病理生理学中起作用的假设。未来的研究有必要证实这些发现并探索潜在的机制。