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

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 ma...

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Bibliographic Details
Published in:NeuroImage clinical 2014-01, Vol.4 (C), p.326-335
Main Authors: Coplan, Jeremy D, Fathy, Hassan M, Abdallah, Chadi G, Ragab, Sherif A, Kral, John G, Mao, Xiangling, Shungu, Dikoma C, Mathew, Sanjay J
Format: Article
Language:English
Subjects:
Adult
Anxiety Disorders - diagnosis
Anxiety Disorders - metabolism
Aspartic Acid - analogs & derivatives
Aspartic Acid - metabolism
Biomarkers - metabolism
Body mass index
Creatine (CR)
Down-Regulation
Female
Generalized anxiety disorder
Hippocampus - metabolism
Humans
Magnetic Resonance Imaging - methods
Male
Neuronal integrity
Obesity
Overweight - diagnosis
Overweight - metabolism
Penn State Worry Questionnaire
Proton Magnetic Resonance Spectroscopy - methods
Reproducibility of Results
Sensitivity and Specificity
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Summary: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). We combined two previously studied cohorts of GAD and control subjects. Using proton magnetic resonance spectroscopy imaging ((1)H 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. Overweight subjects (BMI ≥ 25) exhibited lower NAA levels in the hippocampus than normal-weight subjects (BMI 
ISSN:2213-1582
2213-1582
DOI:10.1016/j.nicl.2013.12.014