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NeuroImage Clin:揭示个体过重或影响其大脑细胞的健康

  1. BMI
  2. N-乙酰基-天冬氨酸分子
  3. NAA
  4. 大脑细胞
  5. 过重

来源:生物谷 2014-02-12 23:12

来自纽约州立大学下州医学中心(SUNY Downstate Medical Center)的研究人员通过研究表示,个体过重或许和机体大脑海马体细胞健康相关的分子水平下降直接相关。

2014年2月13日 讯 /生物谷BIOON/ --近日,刊登在国际杂志Neuroimage:Clinical上的一篇研究论文中,来自纽约州立大学下州医学中心(SUNY Downstate Medical Center)的研究人员通过研究表示,个体过重或许和机体大脑海马体细胞健康相关的分子水平下降直接相关。

文章中,研究者利用磁共振波谱学技术对N-乙酰基-天冬氨酸分子(NAA)进行研究,该分子和大脑细胞健康直接相关,相比正常个体来讲,过重的个体往往表现出较低水平的NAA,而这种效应并不依赖于年龄、性别以及精神病学诊断信息等。

大脑海马体结构是一个类似于海马形状的大脑结构,其对于信息的储存以及情感控制至关重要,研究者Coplan博士表示,这项研究显示,过重和大脑脑细胞的健康程度相关,而这项研究也被认为是首次对机体NAA和体重关系的一项研究。

不论NAA是否是过重导致的,引发个体过重的原因尚不清楚,未来还需要进行大量研究来解释是否体重降低可以导致NAA水平的增加。最后研究者说道,我们的研究也发现过度担忧的情绪也会降低海马体产生NAA分子,但是过度担忧和过重并不相关。正常的BMI(体重指数)应该为18.5-24.9之间,处于25-29.9之间则为过重,而肥胖个体的BMI值一般在30及30以上。(生物谷Bioon.com)

Reduced hippocampal N-acetyl-aspartate (NAA) as a biomarker for overweight ☆

Jeremy D. Coplana, , Hassan M. Fathya, Chadi G. Abdallahb, Sherif A. Ragaba, John G. Kralc, Xiangling Maod, e, f, Dikoma C. Shungud, e, f, Sanjay J. Mathewg

Objective We previously demonstrated an inverse relationship between both dentate gyrus neurogenesis – a form of neuroplasticity – and expression of the antiapoptotic gene marker, BCL-2 and adult macaque body weight. We therefore explored whether a similar inverse correlation existed in humans between body mass index (BMI) and hippocampal N-acetyl-aspartate (NAA), a marker of neuronal integrity and putatively, neuroplasticity. We also studied the relationship of a potentially neurotoxic process, worry, to hippocampal NAA in patients with generalized anxiety disorder (GAD) and control subjects (CS). Methods We combined two previously studied cohorts of GAD and control subjects. Using proton magnetic resonance spectroscopy imaging (1H MRSI) in medication-free patients with GAD (n = 29) and a matched healthy control group (n = 22), we determined hippocampal concentrations of (1) NAA (2) choline containing compounds (CHO), and (3) Creatine + phosphocreatine (CR). Data were combined from 1.5 T and 3 T scans by converting values from each cohort to z-scores. Overweight and GAD diagnosis were used as categorical variables while the Penn State Worry Questionnaire (PSWQ) and Anxiety Sensitivity Index (ASI) were used as dependent variables. Results Overweight subjects (BMI ≥ 25) exhibited lower NAA levels in the hippocampus than normal-weight subjects (BMI < 25) (partial Eta-squared = 0.14) controlling for age, sex and psychiatric diagnosis, and the effect was significant for the right hippocampus in both GAD patients and control subjects. An inverse linear correlation was noted in all subjects between right hippocampal NAA and BMI. High scores on the PSWQ predicted low hippocampal NAA and CR. Both BMI and worry were independent inverse predictors of hippocampal NAA. Conclusion Overweight was associated with reduced NAA concentrations in the hippocampus with a strong effect size. Future mechanistic studies are warranted.

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