Metabolite T1 relaxation times decrease across the adult lifespan

Author:

Murali‐Manohar Saipavitra12ORCID,Gudmundson Aaron T.12,Hupfeld Kathleen E.12ORCID,Zöllner Helge J.12ORCID,Hui Steve C. N.12,Song Yulu12,Simicic Dunja12,Davies‐Jenkins Christopher W.12,Gong Tao34,Wang Guangbin34,Oeltzschner Georg12ORCID,Edden Richard A. E.12

Affiliation:

1. The Russell H. Morgan Department of Radiology and Radiological Science Johns Hopkins University School of Medicine Baltimore Maryland USA

2. F.M. Kirby Research Center for Functional Brain Imaging Kennedy Krieger Institute Baltimore Maryland USA

3. Departments of Radiology Shandong Provincial Hospital Affiliated to Shandong First Medical University Jinan Shandong China

4. Departments of Radiology, Shandong Provincial Hospital Shandong University Jinan Shandong China

Abstract

AbstractRelaxation 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.

Funder

National Center for Advancing Translational Sciences

Publisher

Wiley

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