Irisin is involved in various metabolic pathways and is suggested to be a potential agent capable of preventing onset of Alzheimer's disease (AD) and ameliorating AD neuropathology and cognitive deficits. In the present study, the serum levels of Irisin and Amyloid-β (Aβ) peptides and the neurocognitive performance among obese individuals at genetic risk for AD were investigated. The correlations between Irisin and AD-related neuropathological and neurocognitive indices were also explored. Thirty-two individuals with a family history of AD (ADFH) and obesity (ADFH-obesity group) and 32 controls (ADFH-non-obesity group) were recruited. Circulating levels of Irisin, Aβ peptides, and metabolic biomarkers, as well as neurocognitive performance [e.g., behavior and brain even-related potentials (ERP)] were measured during a visuospatial working memory task. Although the ADFH-obesity group exhibited comparable reaction times, ERP N2 latency and amplitudes, and P3 latency as compared to the ADFH-non-obesity group when performing the cognitive task, they exhibited significantly lower rates of accuracy and smaller P3 amplitudes in the higher memory-load condition, even when controlling for the blood pressure and cardiorespiratory fitness co-variables. The serum levels of leptin, insulin, and glucose, and HOMA-IR were significantly higher in the ADFH-obesity group relative to the ADFH-non-obesity group, but this was not the case for the levels of Aβ1-40 and Aβ1-42. The Irisin levels approached between-group significance. Partial correlations adjusting for cardiorespiratory fitness and blood pressure showed that Irisin levels were positively associated with neurophysiological (i.e., P3 amplitude) performance in the ADFH-obesity group. The Irisin levels were not significantly correlated with the levels of Aβ1-40 and Aβ1-42. ADFH individuals with obesity exhibited neurocognitive deficits when performing the visuospatial working memory task, and serum Irisin levels could be one of the influencing factors. However, the relationship between the circulating levels of Irisin Aβ peptides needs more evidence to support this assumption.

鸢尾素参与各种代谢途径，并被认为是一种能够预防阿尔茨海默病 (AD) 发作和改善 AD 神经病理学和认知缺陷的潜在药物。在本研究中，研究了具有 AD 遗传风险的肥胖个体的鸢尾素和淀粉样蛋白 β (Aβ) 肽的血清水平以及神经认知表现。还探讨了鸢尾素与 AD 相关神经病理学和神经认知指标之间的相关性。招募了 32 名具有 AD (ADFH) 和肥胖家族史的个体（ADFH 肥胖组）和 32 名对照者（ADFH 非肥胖组）。鸢尾素、Aβ 肽和代谢生物标志物的循环水平，以及神经认知性能 [例如，在视觉空间工作记忆任务期间测量行为和大脑偶数相关电位（ERP）]。尽管与 ADFH 非肥胖组相比，ADFH 肥胖组在执行认知任务时表现出相当的反应时间、ERP N2 潜伏期和幅度以及 P3 潜伏期，但他们在较高的认知任务中表现出显着较低的准确率和较小的 P3 幅度。记忆负荷状况，即使在控制血压和心肺适能协变量时也是如此。与 ADFH 非肥胖组相比，ADFH 肥胖组的瘦素、胰岛素和葡萄糖以及 HOMA-IR 的血清水平显着更高，但 Aβ1-40 和 Aβ1- 水平的情况并非如此。 42. 鸢尾素水平接近组间显着性。调整心肺健康和血压的偏相关表明鸢尾素水平与 ADFH 肥胖组的神经生理学（即 P3 振幅）表现呈正相关。鸢尾素水平与 Aβ1-40 和 Aβ1-42 水平无显着相关性。肥胖的 ADFH 个体在执行视觉空间工作记忆任务时表现出神经认知缺陷，血清鸢尾素水平可能是影响因素之一。然而，鸢尾素 Aβ 肽循环水平之间的关系需要更多证据来支持这一假设。肥胖的 ADFH 个体在执行视觉空间工作记忆任务时表现出神经认知缺陷，血清鸢尾素水平可能是影响因素之一。然而，鸢尾素 Aβ 肽循环水平之间的关系需要更多证据来支持这一假设。肥胖的 ADFH 个体在执行视觉空间工作记忆任务时表现出神经认知缺陷，血清鸢尾素水平可能是影响因素之一。然而，鸢尾素 Aβ 肽循环水平之间的关系需要更多证据来支持这一假设。