Midlife body mass index and cerebral metabolism
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Obesity is a pervasive condition associated with increased risk of dementia, cognitive impairment, and cerebral atrophy in later life. Given that the pathophysiology underlying obesity’s impact on the central nervous system is poorly understood, the current study examined the association between body mass index (BMI) and five cerebral metabolites of neurobiological significance: N-acetyl-aspartate (NAA), a marker of neuronal viability; choline-containing compounds, free choline, phosphocholine and glycerophosphocholine (Cho), markers of membrane breakdown and turn over; creatine (Cr), a marker of energy metabolism; myo-inositol (mI), an organic osmolyte and substrate for the synthesis of the secondary messenger, inositol triphosphate; and glutamate (Glu), a marker of excitatory neurotransmission and synaptic integrity. Fifty-five participants, aged 40-60 years, underwent neuropsychological testing, health screen and proton magnetic resonance spectroscopy (1H MRS) of the occipitoparietal grey matter. Concentrations of NAA, Cho, mI, and Glu were calculated as a ratio over Cr and examined in relation to BMI using multivariate multiple regression. Higher BMI was associated with elevations in mI/Cr (F(5,47)=3.583, p=0.008, ß=0.387, p=0.006), independent of age, sex, fasting glucose levels, and systolic blood pressure. The current study found that higher BMI is related to increased concentrations of the organic osmoltye and glial marker myo-inositol, potentially implicating plasma hypertonicity and neuroinflammation as mechanisms underlying obesity-related brain dysfunction. With validation and absolute quantification, studies of neurometabolites may improve identification of the pathological mechanisms underlying obesity’s consequences on cognition.