TY - JOUR
T1 - Association between serum neuron-specific enolase, age, overweight, and structural MRI patterns in 901 subjects
AU - Hoffmann, Johanna
AU - Janowitz, Deborah
AU - Van Der Auwera, Sandra
AU - Wittfeld, Katharina
AU - Nauck, Matthias
AU - Friedrich, Nele
AU - Habes, Mohamad
AU - Davatzikos, Christos
AU - Terock, Jan
AU - Bahls, Martin
AU - Goltz, Annemarie
AU - Kuhla, Angela
AU - Völzke, Henry
AU - Jörgen Grabe, Hans
N1 - Funding Information:
The SHIP is supported by the German Federal Ministry of Education and Research (grants 01ZZ9603, 01ZZ0103, and 01ZZ0403) and the German Research Foundation (DFG; GR 1912/5–1). MRI scans were supported by the Federal Ministry of Education and Research (grant 03ZIK012) and a joint grant from Siemens Healthineers, Erlangen, Germany, and the Federal State of Mecklenburg-West Pomerania. This cohort is part of the Community Medicine Research net (CMR) of the University of Greifswald, which is funded by the German Federal Ministry of Education and Research and the German Ministry of Cultural Affairs, as well as by the Social Ministry of the Federal State of Mecklenburg-West Pomerania. CMR encompasses several research projects that share data from the population-based SHIP. The work is also supported by the German Research Foundation (DFG; GR 1912/5–1) and the Greifswald Approach to Individualized Medicine (GANI_MED) network funded by the Federal Ministry of Education and Research (grant 03IS2061A). We thank all staff members and participants of the SHIP studies. Measurement of NSE levels were financed by the Research Network Community Medicine.
PY - 2017/12/1
Y1 - 2017/12/1
N2 - Serum neuron-specific enolase (sNSE) is considered a marker for neuronal damage, related to gray matter structures. Previous studies indicated its potential as marker for structural and functional damage in conditions with adverse effects to the brain like obesity and dementia. In the present study, we investigated the putative association between sNSE levels, body mass index (BMI), total gray matter volume (GMV), and magnetic resonance imaging-based indices of aging as well as Alzheimer's disease (AD)-like patterns. Subjects/Methods: sNSE was determined in 901 subjects (499 women, 22-81 years, BMI 18-48 kg/m2), participating in a population-based study (SHIP-TREND). We report age-specific patterns of sNSE levels between males and females. Females showed augmenting, males decreasing sNSE levels associated with age (males: p = 0.1052, females: p = 0.0363). sNSE levels and BMI were non-linearly associated, showing a parabolic association and decreasing sNSE levels at BMI values >25 (p = 0.0056). In contrast to our hypotheses, sNSE levels were not associated with total GMV, aging, or AD-like patterns. Pathomechanisms discussed are: sex-specific hormonal differences, neuronal damage/differentiation, or impaired cerebral glucose metabolism. We assume a sex-dependence of age-related effects to the brain. Further, we propose in accordance to previous studies an actual neuronal damage in the early stages of obesity. However, with progression of overweight, we assume more profound effects of excess body fat to the brain.
AB - Serum neuron-specific enolase (sNSE) is considered a marker for neuronal damage, related to gray matter structures. Previous studies indicated its potential as marker for structural and functional damage in conditions with adverse effects to the brain like obesity and dementia. In the present study, we investigated the putative association between sNSE levels, body mass index (BMI), total gray matter volume (GMV), and magnetic resonance imaging-based indices of aging as well as Alzheimer's disease (AD)-like patterns. Subjects/Methods: sNSE was determined in 901 subjects (499 women, 22-81 years, BMI 18-48 kg/m2), participating in a population-based study (SHIP-TREND). We report age-specific patterns of sNSE levels between males and females. Females showed augmenting, males decreasing sNSE levels associated with age (males: p = 0.1052, females: p = 0.0363). sNSE levels and BMI were non-linearly associated, showing a parabolic association and decreasing sNSE levels at BMI values >25 (p = 0.0056). In contrast to our hypotheses, sNSE levels were not associated with total GMV, aging, or AD-like patterns. Pathomechanisms discussed are: sex-specific hormonal differences, neuronal damage/differentiation, or impaired cerebral glucose metabolism. We assume a sex-dependence of age-related effects to the brain. Further, we propose in accordance to previous studies an actual neuronal damage in the early stages of obesity. However, with progression of overweight, we assume more profound effects of excess body fat to the brain.
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U2 - 10.1038/s41398-017-0035-0
DO - 10.1038/s41398-017-0035-0
M3 - Article
C2 - 29217819
AN - SCOPUS:85038087589
VL - 7
JO - Translational Psychiatry
JF - Translational Psychiatry
SN - 2158-3188
IS - 12
M1 - 1272
ER -