TY - JOUR
T1 - Subclinical vascular disease and cerebral glutamate elevation in metabolic syndrome
AU - Haley, Andreana P.
AU - Gonzales, Mitzi M.
AU - Tarumi, Takashi
AU - Tanaka, Hirofumi
N1 - Funding Information:
Disclosures Dr. Haley is funded by the American Heart Association, the American Federation for Aging Research, and the National Institute of Neurological Disorders and Stroke. Ms. Gonzales and Mr. Tarumi reports no disclosures. Dr. Tanaka received research support from the American Heart Association.
Funding Information:
Sources of Funding This study was funded in part by the American Heart Association (09BGIA2060722), the American Federation for Aging Research (8A0024), the National Institute of Neurological Disorders and Stroke (R01NS75565), and the University of Texas at Austin.
PY - 2012/12
Y1 - 2012/12
N2 - Metabolic syndrome (MetS), the co-occurrence of obesity, hypertension, hyperglycemia and dyslipidema, is an important risk factor for diabetes, cardiovascular disease and end-organ damage in the brain. Our goal was to determine if metabolic syndrome (MetS) differentially affects cerebral metabolism in middle-aged adults with varying degrees of subclinical vascular disease. Sixty-five neurologically healthy adults aged 40 to 60 years (19 with MetS and 46 controls) underwent ultrasound examination of carotid artery intima-media thickness (IMT), a measure of peripheral vascular disease, a full neuropsychological evaluation, and a proton magnetic resonance spectroscopy (1H MRS) scan of occipitoparietal grey matter. The Johnson- Neyman technique and pick-a-point approach were used to test if MetS-related neurochemical changes were moderated by IMT. The MetS and control groups were comparable in age, education, gender distribution, average IMT, and cognitive performance. MetS individuals with low IMT values (1 SD below sample mean) demonstrated comparable neurochemical concentrations to the healthy controls (t=-0.21, p00.84, 95 % CI -0.106 to 0.086), while MetS individuals with high IMT values (1 SD above sample mean) exhibited significantly elevated glutamate concentrations (t=2.84, p00.006, 95 % CI 0.038 to 0.220). We found that the level of peripheral atherosclerosis moderated the level of elevation of cerebral glutamate concentrations in patients with MetS. These results suggest that peripheral metabolic dysfunction in midlife likely acts in conjunction with subclinical vascular disease to foster pro-neurotoxic conditions in the central nervous system creating early brain vulnerability.
AB - Metabolic syndrome (MetS), the co-occurrence of obesity, hypertension, hyperglycemia and dyslipidema, is an important risk factor for diabetes, cardiovascular disease and end-organ damage in the brain. Our goal was to determine if metabolic syndrome (MetS) differentially affects cerebral metabolism in middle-aged adults with varying degrees of subclinical vascular disease. Sixty-five neurologically healthy adults aged 40 to 60 years (19 with MetS and 46 controls) underwent ultrasound examination of carotid artery intima-media thickness (IMT), a measure of peripheral vascular disease, a full neuropsychological evaluation, and a proton magnetic resonance spectroscopy (1H MRS) scan of occipitoparietal grey matter. The Johnson- Neyman technique and pick-a-point approach were used to test if MetS-related neurochemical changes were moderated by IMT. The MetS and control groups were comparable in age, education, gender distribution, average IMT, and cognitive performance. MetS individuals with low IMT values (1 SD below sample mean) demonstrated comparable neurochemical concentrations to the healthy controls (t=-0.21, p00.84, 95 % CI -0.106 to 0.086), while MetS individuals with high IMT values (1 SD above sample mean) exhibited significantly elevated glutamate concentrations (t=2.84, p00.006, 95 % CI 0.038 to 0.220). We found that the level of peripheral atherosclerosis moderated the level of elevation of cerebral glutamate concentrations in patients with MetS. These results suggest that peripheral metabolic dysfunction in midlife likely acts in conjunction with subclinical vascular disease to foster pro-neurotoxic conditions in the central nervous system creating early brain vulnerability.
KW - Atherosclerosis
KW - Brain imaging
KW - Carotid ultrasound
KW - Glutamate
KW - MR spectroscopy
KW - Metabolic syndrome
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U2 - 10.1007/s11011-012-9306-x
DO - 10.1007/s11011-012-9306-x
M3 - Article
C2 - 22552897
AN - SCOPUS:84871432789
VL - 27
SP - 513
EP - 520
JO - Metabolic Brain Disease
JF - Metabolic Brain Disease
SN - 0885-7490
IS - 4
ER -