Association of Circulating Brain-Derived Neurotrophic Factor with Cognition among Adult Obese Population

循环脑源性神经营养因子与成年肥胖人群认知功能的关系

阅读:1

Abstract

BACKGROUND: Obesity has a strong association with the risk of developing cognitive impairment and dementia at a later age. Brain-derived neurotrophic factor (BDNF) and its receptor appear to be important components in cognitive function and are also involved in energy homeostasis. The level of circulating BDNF and its association with cognition has yet to be delineated clearly. In this work we studied the association of circulating BDNF with cognition among the adult obese population. METHODS: The study involved 132 healthy participants between 18 and 40 years of age and of both sexes. The participants were categorized into an obesity group (n=66) and a non-obese group (n=66) based on their body mass index (Asian criteria). The level of cognitive performance was assessed by the event-related potentials P300 (ERPs-P300), mini-mental state examination (MMSE), both visual and auditory reaction times (VRT and ART, respectively), and other pen and paper tests related to memory and executive function. Serum BDNF, glycemic and lipid profiles were estimated. RESULTS: We found significant differences in the ERPs-P300 latency (P<0.001) and amplitude (P=0.002) between the non-obese and obese group. The MMSE score was significantly reduced while VRT (P=0.005) and ART (P=0.001) were larger in the obese group. BDNF levels (P<0.001) were significantly reduced and negatively associated with the obese group. ERPs-P300 latency was negatively associated (r=-0.674, P=0.001) whereas amplitude (r=0.507, P<0.001) was positively associated with the BDNF levels in the adult obese population. CONCLUSION: We found reduced circulating BDNF levels in obese adults and that lower BDNF levels were strongly associated with cognitive decline in the obese adult population.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。