TY - JOUR
T1 - Physiological neuronal decline in healthy aging human brain - An in vivo study with MRI and short echo-time whole-brain 1H MR spectroscopic imaging
AU - Ding, Xiao Qi
AU - Maudsley, Andrew A.
AU - Sabati, Mohammad
AU - Sheriff, Sulaiman
AU - Schmitz, Birte
AU - Schütze, Martin
AU - Bronzlik, Paul
AU - Kahl, Kai G.
AU - Lanfermann, Heinrich
N1 - Funding Information:
Grant support: This work was partially supported by Deutsche Forschungsgemeinschaft and by NIH grant R01 EB016064 (A.A.M.).
PY - 2016/8/15
Y1 - 2016/8/15
N2 - Knowledge of physiological aging in healthy human brain is increasingly important for neuroscientific research and clinical diagnosis. To investigate neuronal decline in normal aging brain eighty-one healthy subjects aged between 20 and 70 years were studied with MRI and whole-brain 1H MR spectroscopic imaging. Concentrations of brain metabolites N-acetyl-aspartate (NAA), choline (Cho), total creatine (tCr), myo-inositol (mI), and glutamine+glutamate (Glx) in ratios to internal water, and the fractional volumes of brain tissue were estimated simultaneously in eight cerebral lobes and in cerebellum. Results demonstrated that an age-related decrease in gray matter volume was the largest contribution to changes in brain volume. Both lobar NAA and the fractional volume of gray matter (FVGM) decreased with age in all cerebral lobes, indicating that the decreased NAA was predominantly associated with decreased gray matter volume and neuronal density or metabolic activity. In cerebral white matter Cho, tCr, and mI increased with age in association with increased fractional volume, showing altered cellular membrane turn-over, energy metabolism, and glial activity in human aging white matter. In cerebellum tCr increased while brain tissue volume decreased with age, showing difference to cerebral aging. The observed age-related metabolic and microstructural variations suggest that physiological neuronal decline in aging human brain is associated with a reduction of gray matter volume and neuronal density, in combination with cellular aging in white matter indicated by microstructural alterations and altered energy metabolism in the cerebellum.
AB - Knowledge of physiological aging in healthy human brain is increasingly important for neuroscientific research and clinical diagnosis. To investigate neuronal decline in normal aging brain eighty-one healthy subjects aged between 20 and 70 years were studied with MRI and whole-brain 1H MR spectroscopic imaging. Concentrations of brain metabolites N-acetyl-aspartate (NAA), choline (Cho), total creatine (tCr), myo-inositol (mI), and glutamine+glutamate (Glx) in ratios to internal water, and the fractional volumes of brain tissue were estimated simultaneously in eight cerebral lobes and in cerebellum. Results demonstrated that an age-related decrease in gray matter volume was the largest contribution to changes in brain volume. Both lobar NAA and the fractional volume of gray matter (FVGM) decreased with age in all cerebral lobes, indicating that the decreased NAA was predominantly associated with decreased gray matter volume and neuronal density or metabolic activity. In cerebral white matter Cho, tCr, and mI increased with age in association with increased fractional volume, showing altered cellular membrane turn-over, energy metabolism, and glial activity in human aging white matter. In cerebellum tCr increased while brain tissue volume decreased with age, showing difference to cerebral aging. The observed age-related metabolic and microstructural variations suggest that physiological neuronal decline in aging human brain is associated with a reduction of gray matter volume and neuronal density, in combination with cellular aging in white matter indicated by microstructural alterations and altered energy metabolism in the cerebellum.
KW - Choline (Cho)
KW - Glutamate (Glu)
KW - Glutamine (Gln)
KW - Myo-inositol (mI)
KW - N-acetyl-aspartate (NAA)
KW - Neuronal metabolic activity
KW - Normal aging
KW - Total creatine (tCr)
KW - Whole-brain MR spectroscopic imaging
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U2 - 10.1016/j.neuroimage.2016.05.014
DO - 10.1016/j.neuroimage.2016.05.014
M3 - Article
C2 - 27164326
AN - SCOPUS:84973878611
VL - 137
SP - 45
EP - 51
JO - NeuroImage
JF - NeuroImage
SN - 1053-8119
ER -