Metabolite T1 relaxation times decrease across the adult lifespan

Relaxation correction is an integral step in quantifying brain metabolite concentrations measured by in vivo magnetic resonance spectroscopy (MRS). While most quantification routines assume constant T1 relaxation across age, it is possible that aging alters T1 relaxation rates, as is seen for T2 rel...

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Published inNMR in biomedicine Vol. 37; no. 9; pp. e5152 - n/a
Main Authors Murali‐Manohar, Saipavitra, Gudmundson, Aaron T., Hupfeld, Kathleen E., Zöllner, Helge J., Hui, Steve C. N., Song, Yulu, Simicic, Dunja, Davies‐Jenkins, Christopher W., Gong, Tao, Wang, Guangbin, Oeltzschner, Georg, Edden, Richard A. E.
Format Journal Article
LanguageEnglish
Published Oxford Wiley Subscription Services, Inc 01.09.2024
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ISSN0952-3480
1099-1492
1099-1492
DOI10.1002/nbm.5152

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Summary:Relaxation correction is an integral step in quantifying brain metabolite concentrations measured by in vivo magnetic resonance spectroscopy (MRS). While most quantification routines assume constant T1 relaxation across age, it is possible that aging alters T1 relaxation rates, as is seen for T2 relaxation. Here, we investigate the age dependence of metabolite T1 relaxation times at 3 T in both gray‐ and white‐matter‐rich voxels using publicly available metabolite and metabolite‐nulled (single inversion recovery TI = 600 ms) spectra acquired at 3 T using Point RESolved Spectroscopy (PRESS) localization. Data were acquired from voxels in the posterior cingulate cortex (PCC) and centrum semiovale (CSO) in 102 healthy volunteers across 5 decades of life (aged 20–69 years). All spectra were analyzed in Osprey v.2.4.0. To estimate T1 relaxation times for total N‐acetyl aspartate at 2.0 ppm (tNAA2.0) and total creatine at 3.0 ppm (tCr3.0), the ratio of modeled metabolite residual amplitudes in the metabolite‐nulled spectrum to the full metabolite signal was calculated using the single‐inversion‐recovery signal equation. Correlations between T1 and subject age were evaluated. Spearman correlations revealed that estimated T1 relaxation times of tNAA2.0 (rs = −0.27; p < 0.006) and tCr3.0 (rs = −0.40; p < 0.001) decreased significantly with age in white‐matter‐rich CSO, and less steeply for tNAA2.0 (rs = −0.228; p = 0.005) and (not significantly for) tCr3.0 (rs = −0.13; p = 0.196) in graymatter‐rich PCC. The analysis harnessed a large publicly available cross‐sectional dataset to test an important hypothesis, that metabolite T1 relaxation times change with age. This preliminary study stresses the importance of further work to measure age‐normed metabolite T1 relaxation times for accurate quantification of metabolite levels in studies of aging. During MRS quantification, metabolite T1 relaxation times across age are typically assumed as a constant. This can lead to error in quantification values if T1s change with age. Therefore, this study investigates age dependence of metabolite T1 relaxation times using data from 102 healthy volunteers (20–69 years). tNAA2.0 and tCr3.0 showed significantly decreasing T1s with age in the centrum semiovale region. Therefore, this study stresses the importance of considering age‐normed T1s in the quantification of metabolites, especially in aging studies.
Bibliography:Funding information
This work was supported by National Institutes of Health Grants R01 EB016089, R01 EB023963, R21 AG060245, R00 AG062230, K00AG068440, and P41EB031771.
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ISSN:0952-3480
1099-1492
1099-1492
DOI:10.1002/nbm.5152