Noninvasive quantification of ascorbate and glutathione concentration in the elderly human brain; PY2011; USA (美國);_教材_lactate_IR95 IR96_University of Minnesota_

Noninvasive quantification of ascorbate and glutathione concentration in the elderly human brain; PY2011; USA (美國);_教材_lactate_IR95 IR96_University of Minnesota_

Noninvasive quantification of ascorbate and glutathione concentration in the elderly human brain; PY2011; USA (美國);_教材_2025-1031_IR95 IR96_V001R01_

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2025-10-31
Noninvasive quantification of ascorbate and glutathione concentration in the elderly human brain

Noninvasive quantification of ascorbate and glutathione concentration in the elderly human brain

Noninvasive quantification of ascorbate and glutathione concentration in the elderly human brain
Noninvasive quantification of ascorbate and glutathione concentration in the elderly human brain
Noninvasive quantification of ascorbate and glutathione concentration in the elderly human brain
非侵入性量化老年人腦中抗壞血酸與穀胱甘肽濃度

Source or References (資訊來源或是參考的資訊):
https://pmc.ncbi.nlm.nih.gov/articles/PMC3118919/
Info cited on 2025-10-31-WD5 (資訊引用於 中華民國114年西元2025年10月31日) by 湯偉晉 (WeiJin Tang)
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NMR Biomed. Author manuscript; available in PMC: 2012 Aug 1.
Published in final edited form as: NMR Biomed. 2011 Jan 12;24(7):888–894. doi: 10.1002/nbm.1646

Noninvasive quantification of ascorbate and glutathione concentration in the elderly human brain
Noninvasive quantification of ascorbate and glutathione concentration in the elderly human brain
非侵入性量化老年人腦中抗壞血酸與穀胱甘肽濃度

Uzay E Emir a,*, Susan Raatz b,c, Susan McPherson d, James S Hodges e, Carolyn Torkelson f, Pierre Tawfik b, Tonya White g,h, Melissa Terpstra a
Author information
Article notes
Copyright and License information
aCenter for Magnetic Resonance Research, Department of Radiology, University of Minnesota, Minneapolis, MN, USA
bFood Science and Nutrition, University of Minnesota, Minneapolis, MN, USA
cUSDA, Grand Forks Human Nutrition Research Center, Grand Forks, ND, USA
dDepartment of Neurology, University of Minnesota, Minneapolis, MN, USA
eDivision of Biostatistics, University of Minnesota, Minneapolis, MN, USA
fFamily Medicine and Community Health, University of Minnesota, Minneapolis, MN, USA
gDepartment of Psychiatry, University of Minnesota, Minneapolis, MN, USA
hDepartments of Child and Adolescent Psychiatry and Radiology, Erasmus Medical Centre, Rotterdam, the Netherlands
*Correspondence to: U. E. Emir, 2021 6th St SE, Minneapolis, MN 55455, USA. uzay@cmrr.umn.edu
PMCID: PMC3118919  NIHMSID: NIHMS276594  PMID: 21834011
The publisher's version of this article is available at NMR Biomed

Abstract
In this study, ascorbate (Asc) and glutathione (GSH) concentrations were quantified noninvasively using double-edited 1H MRS at 4 T in the occipital cortex of healthy young [age (mean ± standard deviation) = 20.4 ± 1.4 years] and elderly (age = 76.6 ± 6.1 years) human subjects. Elderly subjects had a lower GSH concentration than younger subjects (p < 0.05). The Asc concentration was not significantly associated with age. Furthermore, the lactate (Lac) concentration was higher in elderly than young subjects. Lower GSH and higher Lac concentrations are indications of defective protection against oxidative damage and impaired mitochondrial respiration. The extent to which the observed concentration differences could be associated with physiological differences and methodological artifacts is discussed. In conclusion, GSH and Asc concentrations were compared noninvasively for the first time in young vs elderly subjects.

Keywords: ascorbate, glutathione, lactate, brain, human, aging, MEGA-PRESS, MRS

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Here’s your abstract translated into traditional Chinese, with English first, Chinese second, sentence by sentence as you requested:

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Abstract
摘要

In this study, ascorbate (Asc) and glutathione (GSH) concentrations were quantified noninvasively using double-edited 1H MRS at 4 T in the occipital cortex of healthy young [age (mean ± standard deviation) = 20.4 ± 1.4 years] and elderly (age = 76.6 ± 6.1 years) human subjects.
在本研究中，利用 4 特斯拉的雙重編輯 ^1H 核磁共振光譜（MRS）在健康年輕人 [年齡（平均值 ± 標準差）= 20.4 ± 1.4 歲] 和老年人（年齡 = 76.6 ± 6.1 歲）的大腦枕葉皮層，非侵入性量化了抗壞血酸（Asc）與穀胱甘肽（GSH）的濃度。

Elderly subjects had a lower GSH concentration than younger subjects (p < 0.05).
老年人的 GSH 濃度低於年輕人（p < 0.05）。

The Asc concentration was not significantly associated with age.
抗壞血酸（Asc）的濃度與年齡沒有顯著相關。

Furthermore, the lactate (Lac) concentration was higher in elderly than young subjects.
此外，乳酸（Lac）濃度在老年人中高於年輕人。

Lower GSH and higher Lac concentrations are indications of defective protection against oxidative damage and impaired mitochondrial respiration.
較低的 GSH 與較高的乳酸濃度，顯示對氧化損傷的保護功能受損以及線粒體呼吸功能下降。

The extent to which the observed concentration differences could be associated with physiological differences and methodological artifacts is discussed.
本文討論了觀察到的濃度差異在多大程度上可能與生理差異及方法學偏差有關。

In conclusion, GSH and Asc concentrations were compared noninvasively for the first time in young vs elderly subjects.
總結而言，這是首次以非侵入性方式比較年輕人與老年人大腦中的 GSH 與抗壞血酸（Asc）濃度。

Keywords: ascorbate, glutathione, lactate, brain, human, aging, MEGA-PRESS, MRS
關鍵詞：抗壞血酸、穀胱甘肽、乳酸、大腦、人類、老化、MEGA-PRESS、核磁共振光譜（MRS）

Lactate
乳酸鹽
Lactate (乳酸鹽)
乳酸鹽 (Lactate)

lactic acid
乳酸
lactic acid (乳酸)
乳酸 (lactic acid)

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如果你願意，我可以幫你把這篇整篇摘要排成可直接放入論文或報告的中英文對照格式表格，看起來更專業清晰。

你希望我幫你做嗎？
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INTRODUCTION
Ascorbate (Asc, vitamin C) and glutathione (GSH) are the most concentrated chemical antioxidants in the central nervous system (1). Asc and GSH are scavengers of free radicals formed from the interaction of iron and hydrogen peroxide, and play a major role in cellular detoxification (2). Sodium-dependent maintenance of adequate Asc concentration (3,4) is important throughout life (5,6) to support additional processes, including the healthy development and function of neurons (7), neurotransmission (5), enzyme stabilization (8) and signaling in the inflammatory response (9). Numerous studies suggest that brain Asc and GSH concentrations could be affected by age-related neurological conditions. For example, although a decrease in brain Asc concentration has been consistently reported during development, conflicting evidence has been presented on whether Asc concentration declines after maturation (10). A majority of studies on animals indicate that GSH levels decline in the brain with age (11,12), but there is very little information available concerning the effect of age on human brain Asc (13) and GSH concentrations.
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Of course, WeiJin（偉晉）！以下是您提供的英文摘要逐句翻譯成繁體中文的版本，每句英文後面接上對應的中文：

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INTRODUCTION
引言

Ascorbate (Asc, vitamin C) and glutathione (GSH) are the most concentrated chemical antioxidants in the central nervous system (1).
抗壞血酸（Asc，維生素C）與穀胱甘肽（GSH）是中樞神經系統中濃度最高的化學性抗氧化劑（1）。

Asc and GSH are scavengers of free radicals formed from the interaction of iron and hydrogen peroxide, and play a major role in cellular detoxification (2).
Asc與GSH能清除由鐵與過氧化氫反應所產生的自由基，並在細胞解毒過程中扮演重要角色（2）。

Sodium-dependent maintenance of adequate Asc concentration (3,4) is important throughout life (5,6) to support additional processes, including the healthy development and function of neurons (7), neurotransmission (5), enzyme stabilization (8) and signaling in the inflammatory response (9).
透過鈉離子依賴機制維持足夠的Asc濃度（3,4）在整個生命過程中都十分重要（5,6），以支援其他生理過程，包括神經元的健康發育與功能（7）、神經傳導（5）、酶的穩定性（8），以及在發炎反應中的訊號傳導（9）。

Numerous studies suggest that brain Asc and GSH concentrations could be affected by age-related neurological conditions.
許多研究指出，大腦中Asc與GSH的濃度可能會受到與年齡相關的神經性疾病影響。

For example, although a decrease in brain Asc concentration has been consistently reported during development, conflicting evidence has been presented on whether Asc concentration declines after maturation (10).
例如，雖然多數研究一致報告在發育過程中大腦Asc濃度會下降，但在成熟之後Asc濃度是否持續下降，仍存在相互矛盾的證據（10）。

A majority of studies on animals indicate that GSH levels decline in the brain with age (11,12), but there is very little information available concerning the effect of age on human brain Asc (13) and GSH concentrations.
大多數動物研究顯示，隨著年齡增加，大腦中的GSH濃度會下降（11,12），然而關於年齡對人類大腦中Asc（13）及GSH濃度的影響，目前仍缺乏足夠的資料。

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是否希望我接著幫您翻譯這篇論文的「Methods（方法）」部分呢？
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In MRS, resonances from Asc and GSH are difficult to resolve because of significant spectral overlap with other neurochemicals (14). They can be resolved from overlapping contributions, yet retained in the same double-edited 1H MR spectrum measured from the human brain in vivo (15). Previously reported Asc and GSH concentrations, measured in vivo via LCModel analysis of MEGA-PRESS-edited spectra (MEGA-PRESS, MEGA-point-resolved spectroscopy), were in good agreement with those measured from short-TE 1H MRS in the human brain (15–18) and from high-performance liquid chromatography (HPLC) in the rat brain ex vivo (1,19,20), which suggests that the methodology and stated assumptions on T2 (18) facilitate reliable quantification.

The goal of this study was to quantify Asc and GSH concentrations as a function of age in the human brain. To that end, double editing with (DEW) MEGA-PRESS was used for the detection of Asc and GSH resonances.
##
當然可以，WeiJin（偉晉）！以下是您提供的英文段落逐句對照的中英文翻譯版本：

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In MRS, resonances from Asc and GSH are difficult to resolve because of significant spectral overlap with other neurochemicals (14).
在磁共振波譜（MRS）中，Asc與GSH的共振峰難以解析，因為它們的訊號與其他神經化學物質的光譜有顯著重疊（14）。

They can be resolved from overlapping contributions, yet retained in the same double-edited 1H MR spectrum measured from the human brain in vivo (15).
然而，透過適當的訊號處理方法，可以將它們從重疊的光譜中分離出來，同時保留在人類大腦體內測得的雙重編輯¹H磁共振光譜中（15）。

Previously reported Asc and GSH concentrations, measured in vivo via LCModel analysis of MEGA-PRESS-edited spectra (MEGA-PRESS, MEGA-point-resolved spectroscopy), were in good agreement with those measured from short-TE 1H MRS in the human brain (15–18) and from high-performance liquid chromatography (HPLC) in the rat brain ex vivo (1,19,20), which suggests that the methodology and stated assumptions on T2 (18) facilitate reliable quantification.
先前利用MEGA-PRESS編輯光譜（MEGA-PRESS，MEGA點解析磁共振波譜）並經LCModel分析所測得的體內Asc與GSH濃度，與人類大腦中以短回波時間（short-TE）¹H MRS測得的數值（15–18）以及在離體大鼠大腦中以高效液相層析法（HPLC）測得的結果（1,19,20）相當一致，這顯示該方法及其對T₂的假設（18）能夠提供可靠的定量結果。

The goal of this study was to quantify Asc and GSH concentrations as a function of age in the human brain.
本研究的目的是根據年齡變化，量化人類大腦中Asc與GSH的濃度。

To that end, double editing with (DEW) MEGA-PRESS was used for the detection of Asc and GSH resonances.
為達此目的，本研究使用具雙重編輯功能的MEGA-PRESS（DEW MEGA-PRESS）技術來偵測Asc與GSH的共振訊號。

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是否希望我接著幫您翻譯下一段（例如「Methods」或「Results」部分）？
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METHODS
Protocol
All double-edited spectra were measured using a 4-T, 90-cm-bore magnet (Oxford Magnet Technology, Oxford, UK) interfaced to a Varian INOVA spectrometer (Varian, Palo Alto, CA, USA) and equipped with gradients capable of switching to 40 mT/m in 400 µs (Sonata, Siemens, Erlangen, Germany), and with a surface 1H quadrature transceiver (21). Twenty-two young [age (mean ± standard deviation (SD)) = 20.4 ± 1.4 years] and 22 elderly (age = 76.6 ± 6.1 years) individuals gave informed consent for this study, which was conducted according to procedures approved by the Human Subjects’ Protection Committee at the University of Minnesota. The study was repeated three times in consecutive weeks for five subjects in each age group to evaluate measurement reliability (𝜎2
within, the within-subject variance). Each subject was positioned supine inside the magnet with the radiofrequency (RF) transceiver (21) subjacent to their occipital lobe. To ensure consistency in positioning, the external occipital protuberance, the bridge of the nose and the midline of the chin were used to define the median plane, which was centered in the bore to ensure that the midline of the brain was parallel to the axis of the magnet. To maintain the same inclination, a level meter was placed on the chin and midpoint between the eyebrows. The protocol for each scan began with localizer multislice rapid acquisition with relaxation enhancement (RARE) images (TR = 4.0 s; TE = 60 ms; echo train length, 8; matrix, 256 × 128; two averages; slice thickness, 2 mm; five slices) to select a cubic volume of interest (VOI; 3 × 3 × 3 cm3) centered on the midsagittal plane in the occipital lobe. For the 10 subjects who repeated the study three times each, images measured from the initial scan were used to set the boundaries of the VOI for the repeat studies completed 7 and 14 days after the initial scan. The boundaries of the VOI were traced in all slices to ensure that VOIs were placed in exactly the same location and included the same structural/anatomical landmarks. The adjustment of all first- and second-order shim currents was achieved using the fast automatic shimming technique by mapping along projections (FASTMAP) with echo planar imaging readout (22,23), which resulted in water linewidths of 9 ± 2 Hz (mean ± SD). Localizer images were repeated at the end of the scan session to confirm negligible gross motion.

To control for dietary influence on brain Asc concentration, candidates who consumed fewer than five fruits and vegetables per day (i.e. typical consumption according to the National Center for Chronic Disease Prevention and Health Promotion), and who were willing to refrain from taking vitamin C supplements, were recruited. Candidates with neurological disorders or chronic diseases were excluded. Participants started food records 6 days prior to spectroscopy for the calculation of vitamin C consumption. Three days prior to spectroscopy, subjects began a diet designed to contain the recommended dietary allowance (30 mg of vitamin C/1000 kcal/day). Food was provided for the 3 days prior to spectroscopy, and participants documented their compliance, which was computed as the percentage of calories and vitamin C eaten. To measure blood serum Asc concentration ([Asc]blood) on the same morning as each MR scan (which always began between 09.00 and 12.00 h), 8 mL of whole blood was collected and placed immediately on wet ice. Serum was then separated at 21°C and aliquoted into preservative. Ampoules were submitted frozen (− 70°C) to ARUP Laboratories, Inc. (Salt Lake City, UT, USA) for analysis by spectrophotometry. Three tests for cognitive status were administered to each participant. The Montreal Cognitive Assessment (MoCA) was administered to detect mild cognitive impairment with high sensitivity (24). To detect more subtle changes, timed performances on the symbol digit modalities test (Psychological Assessment Resources, Inc., FL, USA) and on the Trail Making Test (parts A and B) were also evaluated. Each subject completed the Geriatric Depression Scale (25). All measures of vitamin C consumption, compliance to the study diet, [Asc]blood, cognitive status and depression were analyzed for confounding with brain Asc and GSH concentration using linear regression. The significance level for any single association, without correction for multiple comparisons, was set at p < 0.025.

Homonuclear editing
Double editing for Asc and the cysteine residue of GSH (2.95 ppm) was achieved via DEW MEGA-PRESS, as described previously (26). Water suppression using variable-power RF pulses with optimized relaxation delays (VAPOR) (27) and outer volume saturation were applied before the DEW MEGA-PRESS pulse train. Slice-selective excitation was achieved using a 2-ms sinc RF pulse with a bandwidth of 2.0 kHz (γB1 = 706 Hz). Slice-selective refocusing used a 3-ms sinc RF pulse with a bandwidth of 1.5 kHz (γB1 = 942 Hz). Edited spectra were measured as described above (TE = 122 ms; number of excitations = 512; TR = 4.5 s) from the 27-mL VOI. This TE was set to minimize contributions from coedited resonances, such as phosphorylcholine (PC), glycerophosphorylcholine (GPC), myo-inositol (Ins) and N-acetylaspartate (NAA). At this TE, optimal editing efficiency was achieved using a 45-ms Gaussian pulse set at 4.10 ppm for Asc and 4.56 ppm for the cysteine β-CH2 of GSH. The chemical shift for localization was set to 3.26 ppm to minimize the chemical shift displacement artifact for the detection of GSH and Asc. Field drift was monitored to ensure that it did not exceed ± 10 Hz. The entire scan took approximately 1.5 h per session. The spectral width was 6000 Hz and 4035 complex points were acquired for each spectrum. Each single free induction decay (FID) was stored separately in memory, and the frequency and phase were corrected on the basis of the NAA methyl signal prior to summation of all FIDs (28). To ensure a flat baseline, residual unsuppressed water was removed from the spectrum using the Hankel–Lanczos singular value decomposition (HLSVD) (29). Resonances between 4.5 and 4.9 ppm (water = 4.7 ppm), as determined by the HLSVD algorithm, were subtracted from the data.

Quantification
For each subject, the metabolite concentrations were quantified from the DEW MEGA-PRESS-edited spectra using LCModel version 6.2 with optimized parameters for a flat baseline (30). The node spacing was set high using the DKNTMN parameter and the baseline was held flat using the ALPBMN parameter. The following were included in the basis set: Asc, GSH, Ins, lactate (Lac), NAA, PC, GPC, glycerophosphorylethanolamine (GPE) and phosphorylethanolamine (PE). These spectra were simulated using the quantum mechanics density matrix formalism with published values of J-coupling constants and chemical shifts (14,26,31). The accuracy of simulation was verified by ensuring that concentrations quantified using experimentally measured and simulated basis sets were not different (p > 0.05). Concentrations were calculated using tissue water as an internal reference, i.e.

𝐶met=𝑘×
SImet
SIH2⁡O

×[H2⁡O]×
WC
1−𝑓CSF

[1]
where SImet corresponds to the signal intensity of metabolites measured by LCModel and SIH2O is the integral of the water resonance acquired using stimulated echo acquisition mode (STEAM) spectroscopy (TR = 4.5 s, TM = 42 ms, TE = 4 ms). [H2O] denotes the concentration of pure water. WC refers to the water content of the gray matter, and is assumed to be 0.8 (32). The constant k was determined using a phantom experiment in which concentrations of NAA, Asc, GSH and Lac (10 mm) were known. The constant k accounted for the editing efficiency. As the effects of T2 are not accounted for in eqn (1), concentrations are reported in institutional units (i.u.), which are intended to approximate micromoles per gram of brain tissue. Next, the cerebrospinal fluid (CSF) fraction [obtained by fitting integrals of unsuppressed water spectra measured at several TE with a biexponential decay function (33)] in each voxel (fCSF) was used to correct for the partial volume effect, assuming a negligible concentration of metabolites in CSF (34). To account for the high concentration of Lac in CSF, tissue concentrations of Lac were corrected by subtracting the same CSF contribution for young and elderly subjects (35).

The criteria for the reliable quantification of metabolite concentrations were based on negligible fitted residuals and the Cramer–Rao lower bounds (CRLBs), which are estimated SDs, expressed as a percentage of the estimated concentrations (36). Concentrations with CRLB > 50% were classified as not detected. Only metabolites for which CRLBs were below 50% in at least half of the spectra were reported.

Statistical methods
The concentrations of metabolites in young and elderly subjects were compared using a two-tailed, unpaired, Student’s t-test without correction for multiple comparisons. For the five subjects in each age group who underwent three repeat studies, the average of the three studies was used as a single measurement for the statistical analysis. To examine measurement reliability, a mathematical model was built to describe the contributions of between-subject (interindividual) and within-subject (intraindividual) variation. The overall measurement variance (SD squared) in one measurement can be expressed as 𝜎2=𝜎2
s−s+𝜎2
within. The information about 𝜎2
within, the within-subject variance, came from the 10 repeat studies, whereas all 44 subjects provided information about 𝜎2
s−s the within-subject variance. Variance components were estimated by maximizing the restricted likelihood.

RESULTS
Figure 1 compares the representative double-edited spectra measured from young and elderly subjects. The double-edited spectra are characterized by several major peaks, including Asc at 3.73 ppm, GSH at 2.95 ppm and Lac at 1.33 ppm. Less intense GSH and more intense Lac resonances are discernible in the spectrum measured from elderly subjects.

Figure 1.
Figure 1

Open in a new tab
Representative double editing with MEGA-point-resolved spectroscopy (DEW MEGA-PRESS) spectra (TE = 122 ms; TR = 4.5 s; number of excitations = 512) from one young (left) and one elderly (right) subject. Constancy or differences in ascorbate (Asc) (3.73 ppm), glutathione (GSH) (2.95 ppm) and lactate (Lac) (1.33 ppm) resonances are illustrated with horizontal broken lines. Gaussian filtering with σ = 0.15 s was applied. Spectra are scaled such that the heights of the Asc peaks are equal. The zero level is indicated by a gray horizontal line. Top: transverse MRI illustrating (box) the location of the volume of interest in the occipital lobe. GPE, glycerophosphorylethanolamine; Ins, myo-inositol; NAA, N-acetylaspartate.

Figure 2 illustrates a representative Asc and GSH double-edited spectrum from one of the young subjects and the output of LCModel analysis that was used to quantify concentrations. Although CRLBs for Ins and NAA were less than 20%, they were classified as not detected because of the large fitted residuals (Fig. 2). Mean metabolite concentrations for each study group are reported in Table 1. The GSH concentration was lower (p = 0.000002) and the Lac concentration was higher (p = 0.0006) in elderly subjects. Asc was not associated with age. Figure 3 displays the concentrations of Asc, GSH and Lac from each subject as a function of age, together with means and SDs. Table 2 details the contributions of the between-subject and within-subject variation to the overall measurement variance in Asc and GSH concentrations.

Figure 2.
Figure 2

Open in a new tab
A representative result of quantification via LCModel. In vivo: edited spectrum. LCModel: overall fit of the edited spectrum; fitted components for ascorbate (Asc), glutathione (GSH), N-acetylaspartate (NAA), lactate (Lac), myo-inositol (Ins), phosphorylcholine (PC), phosphorylethanolamine (PE), glycerophosphorylcholine (GPC) and glycerophosphorylethanolamine (GPE); baseline component of LCModel fitting and fitted residual.

Table 1.
Metabolite concentrations (mean ± standard deviation) in young and elderly subjects. Institutional units (i.u.) estimate the number of micromoles per gram wet weight without correction for T2

Ascorbate (i.u.)   Glutathione (i.u.)a         Lactate (i.u.)a
Young         0.72 ± 0.16 0.31 ± 0.05 0.96 ± 0.14
Elderly        0.78 ± 0.19 0.20 ± 0.08 1.26 ± 0.36
Open in a new tab
ap < 0.05.
Figure 3.
Figure 3

Open in a new tab
Concentrations of ascorbate (Asc) (top), glutathione (GSH) (middle) and lactate (Lac) (bottom) by age group, together with means (boxes) and standard deviations (error bars). Concentrations were quantified in institutional units (i.u.) which were designed to estimate the concentration (µmol/g wet weight) without correction for T2. Means and standard deviations of the concentrations were intentionally shifted to the left of the mean age of each group for clarity.

Table 2.
Between-subject (σs–s) and within-subject (σwithin) variance of ascorbate (Asc) and glutathione (GSH) expressed in terms of standard deviation (square root of variance)

Ascorbate  Glutathione
σs–s   0.14  0.05
σwithin        0.10  0.05
Open in a new tab
Figure 4 shows the difference in CSF fraction (fcsf) between young and elderly subjects in the occipital cortex. The CSF fraction in elderly subjects (0.22 ± 0.1, mean ± SD) was higher (p = 0.0000001) than that of young subjects (0.09 ± 0.03), which was expected on the basis of age-related atrophy. The variance in CSF fraction among repeat measurements was less than 10% of the mean CSF fraction for both young and elderly subjects, attesting to the good reproducibility of the VOI positioning.

Figure 4.
Figure 4

Open in a new tab
The voxel fraction of cerebrospinal fluid (fCSF) by age group, together with means (boxes) and standard deviations (error bars). fCSF was significantly higher in elderly subjects (p < 0.05). Means and standard deviations of fCSF were intentionally shifted to the left of the mean age of each group for clarity.

Brain Asc and GSH concentrations were not associated with any measure of vitamin C consumption, compliance with the study diet, [Asc]blood, cognitive status or depression.

DISCUSSION
The main findings of this study were that the GSH concentration was significantly lower in elderly subjects, whereas the concentration of Asc did not differ significantly. Higher Lac concentration was also found in elderly subjects. Furthermore, the CSF fraction was higher in elderly subjects.

A reduction in GSH concentration with increasing age has been reported in several species, including mosquitoes, adult housefly, fruit fly and mouse and rat brain (12,37,38). The GSH concentration in the CSF of humans decreases with aging (39). The finding of a lower GSH concentration in elderly human subjects in this study is consistent with findings from animal studies (40,41), which show deficits in the detoxification of reactive oxygen species in the aging brain (11). GSH is slightly more predominant in glia than in neurons (1), with the extracellular concentration of GSH normally remaining at relatively low levels (11). GSH concentration in the CSF is very low (11). Therefore, signal contributions to the GSH resonance detected in the VOI were predominantly intracellular. A reduction in intracellular GSH concentration with age may signify deficits in the prevention of oxidative damage.
##
當然可以，WeiJin（偉晉）！以下是您提供的「DISCUSSION（討論）」部分逐句對照的中英文翻譯版本：

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DISCUSSION
討論

The main findings of this study were that the GSH concentration was significantly lower in elderly subjects, whereas the concentration of Asc did not differ significantly.
本研究的主要發現是，老年受試者的GSH濃度顯著低於年輕受試者，而Asc濃度則沒有顯著差異。

Higher Lac concentration was also found in elderly subjects.
此外，在老年受試者中也發現乳酸（Lac）濃度較高。

Furthermore, the CSF fraction was higher in elderly subjects.
而且，老年受試者的腦脊髓液（CSF）比例也較高。

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A reduction in GSH concentration with increasing age has been reported in several species, including mosquitoes, adult housefly, fruit fly and mouse and rat brain (12,37,38).
在多種生物中已報告隨年齡增長而出現GSH濃度下降的現象，包括蚊子、成蠅、果蠅，以及小鼠與大鼠的大腦（12,37,38）。

The GSH concentration in the CSF of humans decreases with aging (39).
在人類腦脊髓液中，GSH濃度也會隨著老化而下降（39）。

The finding of a lower GSH concentration in elderly human subjects in this study is consistent with findings from animal studies (40,41), which show deficits in the detoxification of reactive oxygen species in the aging brain (11).
本研究發現老年人GSH濃度較低，與動物實驗的結果一致（40,41），這些研究顯示老化大腦在清除活性氧（ROS）的解毒能力上有所缺陷（11）。

---

GSH is slightly more predominant in glia than in neurons (1), with the extracellular concentration of GSH normally remaining at relatively low levels (11).
GSH在膠質細胞中的含量略高於神經元（1），而其在細胞外的濃度通常維持在相對較低的水平（11）。

GSH concentration in the CSF is very low (11).
在腦脊髓液中的GSH濃度極低（11）。

Therefore, signal contributions to the GSH resonance detected in the VOI were predominantly intracellular.
因此，在測量區域（VOI）中偵測到的GSH共振訊號主要來自細胞內的成分。

A reduction in intracellular GSH concentration with age may signify deficits in the prevention of oxidative damage.
隨年齡增加而出現的細胞內GSH濃度下降，可能意味著抗氧化損傷防禦能力的減弱。

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是否希望我接著幫您翻譯這篇論文的「Conclusion（結論）」部分呢？
##
Published data suggest that the Asc concentration declines with age (42,43). However, it is unclear whether this phenomenon occurs during the process of development or aging, as most previous studies have focused on development. Guinea pig Asc concentration decreased in young animals from the age of 3 to 6 months, but, during the next 3 months, the Asc concentration in these animals remained unchanged (10). Furthermore, postmortem analyses of animals aged between 9 and 42 months showed no difference in Asc concentration in many tissues, including the brain (10). These findings are supported by several other studies of animal brains (44,45). In the present study, human brain Asc concentration did not differ significantly between young and elderly subjects. Asc is localized primarily in neurons (1) and Asc concentrations in extracellular tissue and CSF are very low (8,19). Therefore, the signal contributions to the Asc resonance detected in the VOI were predominantly neuronal. As such, the findings for Asc concentration reflect neuronal status. The existing literature and the constant Asc concentration found in this study suggest that this study’s young cohort had already completed their maturation phase, and thus no reduction in Asc concentration could be observed in the elderly cohort.
##
當然可以，WeiJin（偉晉）！以下是您提供的段落逐句翻譯成繁體中文的對照版本：

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Published data suggest that the Asc concentration declines with age (42,43).
已發表的研究資料顯示，Asc（抗壞血酸）濃度會隨著年齡增加而下降（42,43）。

However, it is unclear whether this phenomenon occurs during the process of development or aging, as most previous studies have focused on development.
然而，目前尚不清楚此現象是發生在發育階段還是老化過程中，因為大多數先前的研究主要集中於發育時期。

Guinea pig Asc concentration decreased in young animals from the age of 3 to 6 months, but, during the next 3 months, the Asc concentration in these animals remained unchanged (10).
在年輕的天竺鼠中，Asc濃度會在3至6個月齡之間下降，但在接下來的3個月內，這些動物的Asc濃度則維持不變（10）。

Furthermore, postmortem analyses of animals aged between 9 and 42 months showed no difference in Asc concentration in many tissues, including the brain (10).
此外，對9至42個月齡動物的死後分析顯示，在包括大腦在內的多種組織中，Asc濃度並無顯著差異（10）。

These findings are supported by several other studies of animal brains (44,45).
這些結果也獲得其他多項動物大腦研究的支持（44,45）。

In the present study, human brain Asc concentration did not differ significantly between young and elderly subjects.
在本研究中，年輕與老年受試者的大腦Asc濃度並無顯著差異。

Asc is localized primarily in neurons (1) and Asc concentrations in extracellular tissue and CSF are very low (8,19).
Asc主要分布於神經元內（1），而其在細胞外組織與腦脊髓液（CSF）中的濃度則非常低（8,19）。

Therefore, the signal contributions to the Asc resonance detected in the VOI were predominantly neuronal.
因此，在測量區域（VOI）中所偵測到的Asc共振訊號主要來自神經元。

As such, the findings for Asc concentration reflect neuronal status.
因此，Asc濃度的變化可被視為神經元狀態的反映。

The existing literature and the constant Asc concentration found in this study suggest that this study’s young cohort had already completed their maturation phase, and thus no reduction in Asc concentration could be observed in the elderly cohort.
現有文獻與本研究中觀察到的穩定Asc濃度共同指出，本研究的年輕受試群體可能已完成成熟階段，因此在老年組中未觀察到Asc濃度的下降。

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是否希望我繼續幫您翻譯這篇論文的最後一段（例如結論或總結）？
##
The present study also found a higher Lac concentration in elderly subjects. Mitochondrial diseases have been shown to elevate MRS-measured cerebral and CSF Lac levels (46,47). Such elevation could be related to local oxidative stress associated with reduced oxygen supply, increased oxygen demand or impairment in oxidative metabolism. Thus, a higher Lac concentration could reflect mitochondrial respiratory chain problems in the elderly brain. Impaired mitochondrial respiration is consistent with deficits in protection against oxidative damage, and therefore with the lower GSH concentration measured in the elderly cohort.

Because methodological limitations could confound age-related differences in measured metabolite concentrations, such limitations were addressed as follows. In this study, cerebral water was used as an internal reference to quantify metabolite concentrations. Water is a better internal reference than NAA because it can be quantified with higher precision (via sensitivity) and greater accuracy, as the extent to which brain NAA concentration remains constant throughout aging is controversial. However, partial volume effects from CSF can diminish this advantage. Cerebral atrophy associated with aging can potentially lead to an overestimation of brain water concentration within the voxel because of the inclusion of CSF, if appropriate correction is not made. In this study, correction was made for cerebral atrophy via measurement of the CSF content in the VOI. The potential decrease in water concentration in gray matter with age could be another limitation of the use of water as an internal reference (48). However, neither biochemical studies ex vivo nor the study of T1 relaxation times in vivo support a significant reduction in gray matter water content with age (48). We have assumed constant water content in gray matter with respect to age (49). Any reduction in gray matter water concentration as a result of aging would lead to an overestimation of the metabolite concentrations in the elderly group.
##
當然可以，WeiJin（偉晉）！以下是您提供的段落逐句對照的中英文翻譯版本：

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The present study also found a higher Lac concentration in elderly subjects.
本研究亦發現老年受試者的乳酸（Lac）濃度較高。

Mitochondrial diseases have been shown to elevate MRS-measured cerebral and CSF Lac levels (46,47).
研究顯示，粒線體疾病會使磁共振波譜（MRS）測得的大腦及腦脊髓液（CSF）中的乳酸濃度升高（46,47）。

Such elevation could be related to local oxidative stress associated with reduced oxygen supply, increased oxygen demand or impairment in oxidative metabolism.
這種乳酸升高可能與局部氧化壓力有關，而該壓力可由氧氣供應不足、氧氣需求增加或氧化代謝受損所引起。

Thus, a higher Lac concentration could reflect mitochondrial respiratory chain problems in the elderly brain.
因此，較高的乳酸濃度可能反映出老年人大腦中粒線體呼吸鏈的功能異常。

Impaired mitochondrial respiration is consistent with deficits in protection against oxidative damage, and therefore with the lower GSH concentration measured in the elderly cohort.
粒線體呼吸受損與抗氧化損傷保護能力下降相一致，因此與老年受試者中觀察到的GSH濃度降低相符。

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Because methodological limitations could confound age-related differences in measured metabolite concentrations, such limitations were addressed as follows.
由於方法學上的限制可能會混淆與年齡相關的代謝物濃度差異，本研究針對這些潛在問題進行了以下處理。

In this study, cerebral water was used as an internal reference to quantify metabolite concentrations.
在本研究中，以大腦中的水作為內部參考物，用來定量代謝物的濃度。

Water is a better internal reference than NAA because it can be quantified with higher precision (via sensitivity) and greater accuracy, as the extent to which brain NAA concentration remains constant throughout aging is controversial.
水比NAA（乙醯天門冬胺酸）更適合作為內部參考，因為水的定量具有更高的精確度（由於靈敏度較高）與準確性，而關於NAA濃度在整個老化過程中是否維持恆定仍具爭議性。

However, partial volume effects from CSF can diminish this advantage.
然而，腦脊髓液（CSF）所造成的部分體積效應可能會削弱這項優勢。

Cerebral atrophy associated with aging can potentially lead to an overestimation of brain water concentration within the voxel because of the inclusion of CSF, if appropriate correction is not made.
與老化相關的腦萎縮若未經適當校正，可能導致體素（voxel）中大腦水濃度被高估，因為其中可能包含CSF的成分。

In this study, correction was made for cerebral atrophy via measurement of the CSF content in the VOI.
在本研究中，透過測量測量區域（VOI）內的CSF含量，對腦萎縮進行了校正。

The potential decrease in water concentration in gray matter with age could be another limitation of the use of water as an internal reference (48).
灰質中水濃度隨年齡可能下降，這也是以水作為內部參考的一項潛在限制（48）。

However, neither biochemical studies ex vivo nor the study of T1 relaxation times in vivo support a significant reduction in gray matter water content with age (48).
然而，無論是離體的生化研究或體內T₁弛豫時間的研究，都未發現灰質水含量隨年齡顯著下降的證據（48）。

We have assumed constant water content in gray matter with respect to age (49).
因此，本研究假設灰質的水含量在不同年齡之間保持不變（49）。

Any reduction in gray matter water concentration as a result of aging would lead to an overestimation of the metabolite concentrations in the elderly group.
若灰質水濃度因老化而降低，則會導致老年組代謝物濃度的高估。

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是否希望我繼續幫您翻譯最後的結論（Conclusion）或摘要總結部分，讓整篇文章的翻譯完整？
##
Another advantage of using water as an internal reference was the measurement at short TE, which minimized the dependence of the reference signal on T2. The concentrations approximated as µmol/g in young subjects in this study were lower ([Asc] = 0.72 ± 0.16 i.u., [GSH] = 0.31 ± 0.05 i.u., mean ± SD) than those quantified previously (26) at TE = 112 ms ([Asc] = 0.84 ± 0.11 µmol/g, [GSH] = 1.02 ± 0.09 µmol/g) when NAA was used as internal reference. Quantification using NAA as internal reference was based on the assumption that differences between the T2 relaxation of NAA and the T2 relaxation of the antioxidant had the same impact on the resonance intensity in vitro and in vivo, i.e. the ratio exp[–TE/T2(NAA)]/exp[–TE/T2(antioxidant)] was approximately the same under in vitro and in vivo conditions. The lower concentrations approximated in the current study probably reflect the actual influence of T2 on the quantification of metabolite concentrations. In particular, the T2 value of GSH in vivo is very short (30).

In addition, differences in T2 with age have the potential to confound the quantification of metabolite concentrations. As atrophy in normal aging involves neuronal shrinkage, as well as axonal and myelin degeneration (50,51), the resulting increase in the fraction of small neurons could lead to shorter metabolite T2 values (52). Furthermore, age-dependent iron deposition has shown a strong correlation with T2 shortening (53). In other words, not accounting for T2 [eqn (1)] could lead to the underestimation of concentrations in the elderly group.
##
當然可以，WeiJin（偉晉）！以下是您提供的這一段英文內容的逐句中英文對照翻譯，保持專業、清晰且忠實於原文：

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Another advantage of using water as an internal reference was the measurement at short TE, which minimized the dependence of the reference signal on T2.
使用水作為內部參考的另一項優點是可以在短回波時間（TE）下進行測量，從而將參考訊號對T₂的依賴性降至最低。

The concentrations approximated as µmol/g in young subjects in this study were lower ([Asc] = 0.72 ± 0.16 i.u., [GSH] = 0.31 ± 0.05 i.u., mean ± SD) than those quantified previously (26) at TE = 112 ms ([Asc] = 0.84 ± 0.11 µmol/g, [GSH] = 1.02 ± 0.09 µmol/g) when NAA was used as internal reference.
本研究中年輕受試者的濃度（以µmol/g為單位近似計算）較先前在TE = 112毫秒時、以NAA作為內部參考所測得的數值（26）更低（本研究中：[Asc] = 0.72 ± 0.16 i.u., [GSH] = 0.31 ± 0.05 i.u., 平均值 ± 標準差；先前研究：[Asc] = 0.84 ± 0.11 µmol/g, [GSH] = 1.02 ± 0.09 µmol/g）。

Quantification using NAA as internal reference was based on the assumption that differences between the T2 relaxation of NAA and the T2 relaxation of the antioxidant had the same impact on the resonance intensity in vitro and in vivo, i.e. the ratio exp[–TE/T2(NAA)]/exp[–TE/T2(antioxidant)] was approximately the same under in vitro and in vivo conditions.
以NAA作為內部參考的定量方法是基於一個假設：即NAA與抗氧化劑之間T₂弛豫時間的差異，對於體外與體內的共振強度具有相同影響。換言之，比例式 exp[–TE/T₂(NAA)] / exp[–TE/T₂(antioxidant)] 在體外與體內條件下大致相同。

The lower concentrations approximated in the current study probably reflect the actual influence of T2 on the quantification of metabolite concentrations.
本研究中所得較低的濃度值可能反映了T₂對代謝物定量結果的實際影響。

In particular, the T2 value of GSH in vivo is very short (30).
特別是，GSH在體內的T₂值非常短（30）。

---

In addition, differences in T2 with age have the potential to confound the quantification of metabolite concentrations.
此外，T₂隨年齡變化的差異也可能干擾代謝物濃度的定量。

As atrophy in normal aging involves neuronal shrinkage, as well as axonal and myelin degeneration (50,51), the resulting increase in the fraction of small neurons could lead to shorter metabolite T2 values (52).
由於正常老化過程伴隨神經元縮小，以及軸突與髓鞘的退化（50,51），因此小型神經元比例的增加可能導致代謝物T₂值縮短（52）。

Furthermore, age-dependent iron deposition has shown a strong correlation with T2 shortening (53).
此外，與年齡相關的鐵沉積現象已被證實與T₂縮短有強烈關聯（53）。

In other words, not accounting for T2 [eqn (1)] could lead to the underestimation of concentrations in the elderly group.
換言之，若未考慮T₂（見公式1），可能會導致對老年組代謝物濃度的低估。

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是否希望我繼續幫您翻譯這篇論文的最後一段（結論 Conclusion），讓整個研究的中英文翻譯完整？
##
Additional mechanisms that could lead to resonance intensity differences between elderly and young subjects include B1 inhomogeneity and the four-compartment artifact that is associated with J modulation (54–56). If water and metabolite signals are evenly distributed throughout the VOI, the constant k in eqn (1) will account for the sensitivity profile and four-compartment artifacts. However, if water and/or metabolite signal contributions are asymmetric, these factors can introduce error to the measured concentration. In this study, the percentage CSF was higher in the elderly, in part as a result of brain shrinkage and widening of the sagittal sinus. This asymmetry overlain with the sensitivity profile and four-compartment artifact regions led to an artifactual 6% lower [GSH]brain and 4% lower [Lac]brain in elderly than in young subjects (Supporting information Fig. S1). Because displacements were small for Asc, [Asc]brain was affected minimally. Therefore, the influence of asymmetric tissue composition on age-associated differences in [Asc]brain, [GSH]brain and [Lac]brain was negligible relative to the scatter in the data (SD, Table 1). Alternatively, the four-compartment artifact could be suppressed with inner volume saturation (55).

The large fitted residuals near the chemical shifts of Ins (1,3CH at 3.52 ppm) and the aspartate moiety of NAA (3CH2 at 2.49 and 2.67 ppm) suggest either inaccurate basis spectra or the presence of compounds that are not accounted for. For example, the aspartyl moiety of N-acetylaspartylglutamate coedits with Asc more efficiently than does the aspartate moiety of NAA. Fortunately, these large residuals are fully resolved from Asc and GSH, and thus have a trivial influence on the quantification of antioxidant concentrations.
##
當然可以，WeiJin（偉晉）！以下是您提供的這段英文內容的逐句中英文對照翻譯，忠實保留專業醫學與磁共振波譜學（MRS）用語的細節：

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Additional mechanisms that could lead to resonance intensity differences between elderly and young subjects include B1 inhomogeneity and the four-compartment artifact that is associated with J modulation (54–56).
造成老年與年輕受試者之間共振強度差異的其他可能機制，還包括 B₁不均勻性 以及與 J調變（J modulation） 有關的 四區室假象（four-compartment artifact）（54–56）。

If water and metabolite signals are evenly distributed throughout the VOI, the constant k in eqn (1) will account for the sensitivity profile and four-compartment artifacts.
如果水與代謝物的訊號在測量區域（VOI）中均勻分布，則公式（1）中的常數 *k* 可用來補償靈敏度分布及四區室假象的影響。

However, if water and/or metabolite signal contributions are asymmetric, these factors can introduce error to the measured concentration.
然而，若水或代謝物的訊號分布不對稱，這些因素可能會在測得的濃度中引入誤差。

In this study, the percentage CSF was higher in the elderly, in part as a result of brain shrinkage and widening of the sagittal sinus.
在本研究中，老年受試者的腦脊髓液（CSF）比例較高，部分原因是大腦萎縮與矢狀竇（sagittal sinus）擴張所致。

This asymmetry overlain with the sensitivity profile and four-compartment artifact regions led to an artifactual 6% lower [GSH]brain and 4% lower [Lac]brain in elderly than in young subjects (Supporting information Fig. S1).
這種不對稱性與靈敏度分布及四區室假象區域的交互作用，導致老年組的大腦GSH濃度（[GSH]brain）人為地比年輕組低約6%，而乳酸濃度（[Lac]brain）則低約4%（見補充資料圖S1）。

Because displacements were small for Asc, [Asc]brain was affected minimally.
由於Asc的訊號位移幅度很小，因此其大腦濃度（[Asc]brain）幾乎未受影響。

Therefore, the influence of asymmetric tissue composition on age-associated differences in [Asc]brain, [GSH]brain and [Lac]brain was negligible relative to the scatter in the data (SD, Table 1).
因此，不對稱的組織組成對[Asc]brain、[GSH]brain與[Lac]brain的年齡相關差異影響甚微，與資料的離散程度（標準差，見表1）相比可以忽略不計。

Alternatively, the four-compartment artifact could be suppressed with inner volume saturation (55).
另一種方式是可利用內體積飽和（inner volume saturation）技術來抑制四區室假象（55）。

---

The large fitted residuals near the chemical shifts of Ins (1,3CH at 3.52 ppm) and the aspartate moiety of NAA (3CH₂ at 2.49 and 2.67 ppm) suggest either inaccurate basis spectra or the presence of compounds that are not accounted for.
在肌醇（Ins）的化學位移（1,3CH於3.52 ppm）以及NAA的天門冬胺酸部分（3CH₂於2.49與2.67 ppm）附近觀察到較大的擬合殘差，這暗示可能存在基準光譜不準確或未納入分析的化合物。

For example, the aspartyl moiety of N-acetylaspartylglutamate coedits with Asc more efficiently than does the aspartate moiety of NAA.
例如，N-乙醯天門冬胺酸麩胺酸（N-acetylaspartylglutamate, NAAG）的天門冬醯基部分與Asc的共編輯效率高於NAA的天門冬胺酸部分。

Fortunately, these large residuals are fully resolved from Asc and GSH, and thus have a trivial influence on the quantification of antioxidant concentrations.
所幸，這些較大的殘差峰與Asc及GSH的訊號完全區分開，因此對抗氧化劑濃度的定量影響極小，可忽略不計。

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是否希望我接著幫您翻譯這篇論文的最後一節（例如 Conclusion 或 Summary），讓整篇討論區段完整結束？
##
CONCLUSIONS
Differences in the concentrations of two important antioxidants in the elderly human brain have been measured for the first time using noninvasive methods. The GSH concentration was found to be lower in elderly subjects, although a shorter T2 of GSH in the elderly would also lead to this finding. Moreover, the Asc concentration did not differ between young and elderly subjects, provided that the assumptions on Asc T2 are valid. These results provide an insight into the association between age-related neurodegeneration and oxidative stress.
##
當然可以，WeiJin（偉晉）！以下是這段 「CONCLUSIONS」結論部分 的英文與繁體中文逐句對照翻譯：

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CONCLUSIONS
結論

Differences in the concentrations of two important antioxidants in the elderly human brain have been measured for the first time using noninvasive methods.
本研究首次利用非侵入性方法測量出老年人腦中兩種重要抗氧化劑濃度的差異。

The GSH concentration was found to be lower in elderly subjects, although a shorter T2 of GSH in the elderly would also lead to this finding.
研究發現，老年受試者的穀胱甘肽（GSH）濃度較低，但此結果也可能部分反映出老年人GSH的T₂值較短所造成的影響。

Moreover, the Asc concentration did not differ between young and elderly subjects, provided that the assumptions on Asc T2 are valid.
此外，在假設抗壞血酸（Asc）的T₂值設定正確的前提下，年輕組與老年組之間的Asc濃度並無顯著差異。

These results provide an insight into the association between age-related neurodegeneration and oxidative stress.
這些結果為年齡相關性神經退化與氧化壓力之間的關聯提供了新的見解。

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是否希望我幫您把整篇摘要（從開頭到結論）整理成完整的中英對照格式（排版整齊、方便閱讀或列印）？這樣您可以一次保存整篇譯文。
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Supplementary Material
Supp Data
NIHMS276594-supplement-Supp_Data.doc (16.5KB, doc)
Acknowledgements
We thank Pierre-Gilles Henry and Dinesh Deelchand for developing the software for LCModel analysis of the edited spectra and simulation. We thank Ivan Tkac for MRS-related advice throughout the project. We appreciate the professionalism with which nutrition and nursing staff at the Clinical and Translational Science Unit, University of Minnesota, executed this protocol. We thank Dianne Hutter, RN for assistance with administering the protocol and managing blood samples, the University of Minnesota Alumni Association and the Metropolitan Area Agency on Aging (MAAA) for assistance in recruiting elderly subjects, and colleagues at the Center for Magnetic Resonance Research (CMRR) for maintaining spectrometer performance.

This work was supported by the National Institutes of Health through grant numbers R21-AG029582, P41-RR008079, P30-NS057091, M01-RR00400 and S10 RR023730.

Abbreviations used
Asc
ascorbate
[Asc]blood
blood serum ascorbate concentration
Cho
choline
Cr
creatine
CRLB
Cramer–Rao lower bound
CSF
cerebrospinal fluid
DEW MEGA-PRESS
double editing with MEGA-point-resolved spectroscopy
FASTMAP
fast automatic shimming technique by mapping along projections
fCSF
cerebrospinal fluid fraction
FID
free induction decay
GPC
glycerophosphorylcholine
GPE
glycerophosphoryl-ethanolamine
GSH
glutathione
HLSVD
Hankel–Lanczos singular value decomposition
Ins
myo-inositol
Lac
lactate
MoCA
the Montreal Cognitive Assessment
NAA
N-acetylaspartate
OVS
outer volume suppression
PC
phosphorylcholine
PE
phosphorylethanolamine
RARE
rapid acquisition with relaxation enhancement
RF
radiofrequency
SD
standard deviation
SNR
signal-to-noise ratio
STEAM
stimulated echo acquisition mode
VAPOR
variable-power radiofrequency pulses with optimized relaxation delays
VOI
volume of interest
##
好的，WeiJin（偉晉）！以下是您提供的縮寫清單（Abbreviations）的中英文逐句對照翻譯版本，保持專業醫學術語：

---

Asc
抗壞血酸（ascorbate）

[Asc]blood
血清抗壞血酸濃度（blood serum ascorbate concentration）

Cho
膽鹼（choline）

Cr
肌酸（creatine）

CRLB
克拉美–羅下界（Cramer–Rao lower bound）

CSF
腦脊髓液（cerebrospinal fluid）

DEW MEGA-PRESS
雙重編輯MEGA點解析光譜（double editing with MEGA-point-resolved spectroscopy）

FASTMAP
沿投影快速自動調勻技術（fast automatic shimming technique by mapping along projections）

fCSF
腦脊髓液比例（cerebrospinal fluid fraction）

FID
自由感應衰減（free induction decay）

GPC
甘油磷酸膽鹼（glycerophosphorylcholine）

GPE
甘油磷酸乙醇胺（glycerophosphoryl-ethanolamine）

GSH
穀胱甘肽（glutathione）

HLSVD
Hankel–Lanczos奇異值分解（Hankel–Lanczos singular value decomposition）

Ins
肌醇（myo-inositol）

Lac
乳酸（lactate）

MoCA
蒙特利爾認知評估（the Montreal Cognitive Assessment）

NAA
乙醯天門冬胺酸（N-acetylaspartate）

OVS
外體積抑制（outer volume suppression）

PC
磷酸膽鹼（phosphorylcholine）

Phosphorylcholine
磷酸膽鹼
Phosphorylcholine (磷酸膽鹼)
磷酸膽鹼 (Phosphorylcholine)

PE
磷酸乙醇胺（phosphorylethanolamine）

Phosphorylethanolamine
磷酸乙醇胺
Phosphorylethanolamine (磷酸乙醇胺)
磷酸乙醇胺 (Phosphorylethanolamine)

RARE
快速弛豫增強獲取（rapid acquisition with relaxation enhancement）

RF
射頻（radiofrequency）

Radiofrequency
射頻
Radiofrequency (射頻)
射頻 (Radiofrequency)

SD
標準差（standard deviation）

SNR
訊號雜訊比（signal-to-noise ratio）

STEAM
受激回聲獲取模式（stimulated echo acquisition mode）

VAPOR
變功率射頻脈衝優化弛豫延遲（variable-power radiofrequency pulses with optimized relaxation delays）

VOI
測量區域（volume of interest）

---

如果您願意，我可以幫您把整篇英文摘要連同翻譯、討論、結論與縮寫整理成完整的中英對照文件，排版整齊，方便學術引用或列印。

您希望我直接幫您整理嗎？
##
Footnotes
Supporting information may be found in the online version of this article.

REFERENCES
1.Rice ME, Russo-Menna I. Differential compartmentalization of brain ascorbate and glutathione between neurons and glia. Neuroscience. 1998;82(4):1213–1223. doi: 10.1016/s0306-4522(97)00347-3. [DOI] [PubMed] [Google Scholar]
2.Rice ME, Forman RE, Chen BT, Avshalumov MV, Cragg SJ, Drew KL. Brain antioxidant regulation in mammals and anoxia-tolerant reptiles: balanced for neuroprotection and neuromodulation. Comp. Biochem. Physiol. C: Toxicol. Pharmacol. 2002;133(4):515–525. doi: 10.1016/s1532-0456(02)00116-3. [DOI] [PubMed] [Google Scholar]
3.Hediger MA. New view at C. Nat. Med. 2002;8(5):445–446. doi: 10.1038/nm0502-445. [DOI] [PubMed] [Google Scholar]
4.Spector R. Nutrient transport systems in brain: 40 years of progress. J. Neurochem. 2009;111(2):315–320. doi: 10.1111/j.1471-4159.2009.06326.x. [DOI] [PubMed] [Google Scholar]
5.Harrison FE, Hosseini AH, McDonald MP, May JM. Vitamin C reduces spatial learning deficits in middle-aged and very old APP/PSEN1 transgenic and wild-type mice. Pharmacol. Biochem. Behav. 2009;93(4):443–450. doi: 10.1016/j.pbb.2009.06.006. [DOI] [PMC free article] [PubMed] [Google Scholar]
6.Tveden-Nyborg P, Johansen LK, Raida Z, Villumsen CK, Larsen JO, Lykkesfeldt J. Vitamin C deficiency in early postnatal life impairs spatial memory and reduces the number of hippocampal neurons in guinea pigs. Am. J. Clin. Nutr. 2009;90(3):540–546. doi: 10.3945/ajcn.2009.27954. [DOI] [PubMed] [Google Scholar]
7.Qiu S, Li L, Weeber EJ, May JM. Ascorbate transport by primary cultured neurons and its role in neuronal function and protection against excitotoxicity. J. Neurosci. Res. 2007;85(5):1046–1056. doi: 10.1002/jnr.21204. [DOI] [PubMed] [Google Scholar]
8.Harrison FE, May JM. Vitamin C function in the brain: vital role of the ascorbate transporter SVCT2. Free Radic. Biol. Med. 2009;46(6):719–730. doi: 10.1016/j.freeradbiomed.2008.12.018. [DOI] [PMC free article] [PubMed] [Google Scholar]
9.Casetta I, Govoni V, Granieri E. Oxidative stress, antioxidants and neurodegenerative diseases. Curr. Pharm. Des. 2005;11(16):2033–2052. doi: 10.2174/1381612054065729. [DOI] [PubMed] [Google Scholar]
10.Lykkesfeldt J, Moos T. Age-dependent change in vitamin C status: a phenomenon of maturation rather than of ageing. Mech. Ageing Dev. 2005;126(8):892–898. doi: 10.1016/j.mad.2005.03.010. [DOI] [PubMed] [Google Scholar]
11.Janáky R, Cruz-Aguado R, Oja S, Shaw C. 15 Glutathione in the nervous system: roles in neural function and health and implications for neurological disease. In: Lajtha A, editor. Handbook of Neurochemistry and Molecular Neurobiology. 3rd ed. Springer: New York; 2007. pp. 347–399. [Google Scholar]
12.Maher P. The effects of stress and aging on glutathione metabolism. Ageing Res. Rev. 2005;4(2):288–314. doi: 10.1016/j.arr.2005.02.005. [DOI] [PubMed] [Google Scholar]
13.Schaus R. The ascorbic acid content of human pituitary, cerebral cortex, heart, and skeletal muscle and its relation to age. Am. J. Clin. Nutr. 1957;5(1):39–41. doi: 10.1093/ajcn/5.1.39. [DOI] [PubMed] [Google Scholar]
14.Govindaraju V, Young K, Maudsley AA. Proton NMR chemical shifts and coupling constants for brain metabolites. NMR Biomed. 2000;13(3):129–153. doi: 10.1002/1099-1492(200005)13:3<129::aid-nbm619>3.0.co;2-v. [DOI] [PubMed] [Google Scholar]
15.Terpstra M, Marjanska M, Henry PG, Tkac I, Gruetter R. Detection of an antioxidant profile in the human brain in vivo via double editing with MEGA-PRESS. Magn. Reson. Med. 2006;56(6):1192–1199. doi: 10.1002/mrm.21086. [DOI] [PubMed] [Google Scholar]
16.Terpstra M, Henry PG, Gruetter R. Measurement of reduced glutathione (GSH) in human brain using LCModel analysis of difference-edited spectra. Magn. Reson. Med. 2003;50(1):19–23. doi: 10.1002/mrm.10499. [DOI] [PubMed] [Google Scholar]
17.Tkáč I, Öz G, Adriany G, Uğurbil K, Gruetter R. In vivo 1H NMR spectroscopy of the human brain at high magnetic fields: metabolite quantification at 4T vs.7T. Magn. Reson. Med. 2009;62(4):868–879. doi: 10.1002/mrm.22086. [DOI] [PMC free article] [PubMed] [Google Scholar]
18.Terpstra M, Uğurbil K, Tkáč I. Noninvasive quantification of human brain ascorbate concentration using 1H NMR spectroscopy at 7 T. NMR Biomed. 2010;23(3):227–232. doi: 10.1002/nbm.1423. [DOI] [PMC free article] [PubMed] [Google Scholar]
19.Rice ME. Ascorbate regulation and its neuroprotective role in the brain. Trends Neurosci. 2000;23(5):209–216. doi: 10.1016/s0166-2236(99)01543-x. [DOI] [PubMed] [Google Scholar]
20.Terpstra M, Tkac I, Rao R, Gruetter R. Quantification of vitamin C in the rat brain in vivo using short echo-time 1H MRS. Magn. Reson. Med. 2006;55(5):979–983. doi: 10.1002/mrm.20854. [DOI] [PubMed] [Google Scholar]
21.Adriany G, Gruetter R. A half-volume coil for efficient proton decoupling in humans at 4 tesla. J. Magn. Reson. 1997;125(1):178–184. doi: 10.1006/jmre.1997.1113. [DOI] [PubMed] [Google Scholar]
22.Gruetter R, Tkáč I. Field mapping without reference scan using asymmetric echo-planar techniques. Magn. Reson. Med. 2000;43(2):319–323. doi: 10.1002/(sici)1522-2594(200002)43:2<319::aid-mrm22>3.0.co;2-1. [DOI] [PubMed] [Google Scholar]
23.Gruetter R. Automatic, localized in vivo adjustment of all first- and second-order shim coils. Magn. Reson. Med. 1993;29(6):804–811. doi: 10.1002/mrm.1910290613. [DOI] [PubMed] [Google Scholar]
24.Nasreddine ZS, Phillips NA, Bedirian V, Charbonneau S, Whitehead V, Collin I, Cummings JL, Chertkow H. The Montreal Cognitive Assessment, MoCA: a brief screening tool for mild cognitive impairment. J. Am. Geriatr. Soc. 2005;53(4):695–699. doi: 10.1111/j.1532-5415.2005.53221.x. [DOI] [PubMed] [Google Scholar]
25.Onishi J, Suzuki Y, Umegaki H, Endo H, Kawamura T, Iguchi A. A comparison of depressive mood of older adults in a community, nursing homes, and a geriatric hospital: factor analysis of Geriatric Depression Scale. J. Geriatr. Psychiatry Neurol. 2006;19(1):26–31. doi: 10.1177/0891988705284725. [DOI] [PubMed] [Google Scholar]
26.Terpstra M, Marjanska M, Henry PG, Tkáč I, Gruetter R. Detection of an antioxidant profile in the human brain in vivo via double editing with MEGA-PRESS. Magn. Reson. Med. 2006;56(6):1192–1199. doi: 10.1002/mrm.21086. [DOI] [PubMed] [Google Scholar]
27.Tkac I, Starcuk Z, Choi IY, Gruetter R. In vivo 1H NMR spectroscopy of rat brain at 1ms echo time. Magn. Reson. Med. 1999;41(4):649–656. doi: 10.1002/(sici)1522-2594(199904)41:4<649::aid-mrm2>3.0.co;2-g. [DOI] [PubMed] [Google Scholar]
28.Terpstra M, Uğurbil K, Gruetter R. Direct in vivo measurement of human cerebral GABA concentration using MEGA-editing at 7 Tesla. Magn. Reson. Med. 2002;47(5):1009–1012. doi: 10.1002/mrm.10146. [DOI] [PubMed] [Google Scholar]
29.Cabanes E, Confort-Gouny S, Le Fur Y, Simond G, Cozzone PJ. Optimization of residual water signal removal by HLSVD on simulated short echo time proton MR spectra of the human brain. J. Magn. Reson. 2001;150(2):116–125. doi: 10.1006/jmre.2001.2318. [DOI] [PubMed] [Google Scholar]
30.Emir UE, Deelchand D, Henry PG, Terpstra M. Noninvasive quantification of T(2) and concentrations of ascorbate and glutathione in the human brain from the same double-edited spectra. NMR Biomed. 2010 doi: 10.1002/nbm.1583. [DOI] [PMC free article] [PubMed] [Google Scholar]
31.Henry PG, Marjanska M, Walls JD, Valette J, Gruetter R, Ugurbil K. Proton-observed carbon-edited NMR spectroscopy in strongly coupled second-order spin systems. Magn. Reson. Med. 2006;55(2):250–257. doi: 10.1002/mrm.20764. [DOI] [PubMed] [Google Scholar]
32.Siegel GJ, editor. Basic Neurochemistry: Molecular, Cellular and Medical Aspects. Philadelphia: Lippincott-Raven Publishers; 1999. [Google Scholar]
33.Ernst T, Kreis R, Ross BD. Absolute quantitation of water and metabolites in the human brain. I. Compartments and water. J. Magn. Reson., Ser. B. 1993;102(1):1–8. [Google Scholar]
34.Kruse T, Reiber H, Neuhoff V. Amino acid transport across the human blood-CSF barrier. An evaluation graph for amino acid concentrations in cerebrospinal fluid. J. Neurol. Sci. 1985;70(2):129–138. doi: 10.1016/0022-510x(85)90082-6. [DOI] [PubMed] [Google Scholar]
35.Regenold WT, Phatak P, Marano CM, Sassan A, Conley RR, Kling MA. Elevated cerebrospinal fluid lactate concentrations in patients with bipolar disorder and schizophrenia: implications for the mitochondrial dysfunction hypothesis. Biol. Psychiatry. 2009;65(6):489–494. doi: 10.1016/j.biopsych.2008.11.010. [DOI] [PMC free article] [PubMed] [Google Scholar]
36.Provencher SW. Estimation of metabolite concentrations from localized in vivo proton NMR spectra. Magn. Reson. Med. 1993;30(6):672–679. doi: 10.1002/mrm.1910300604. [DOI] [PubMed] [Google Scholar]
37.Sohal RS, Weindruch R. Oxidative stress, caloric restriction, and aging. Science. 1996;273(5271):59–63. doi: 10.1126/science.273.5271.59. [DOI] [PMC free article] [PubMed] [Google Scholar]
38.Sohal RS, Sohal BH, Brunk UT. Relationship between antioxidant defenses and longevity in different mammalian species. Mech. Ageing Dev. 1990;53(3):217–227. doi: 10.1016/0047-6374(90)90040-m. [DOI] [PubMed] [Google Scholar]
39.Cudkowicz ME, Sexton PM, Ellis T, Hayden DL, Gwilt PR, Whalen J, Brown RH., Jr The pharmacokinetics and pharmaco-dynamics of procysteine in amyotrophic lateral sclerosis. Neurology. 1999;52(7):1492–1494. doi: 10.1212/wnl.52.7.1492. [DOI] [PubMed] [Google Scholar]
40.Hazelton GA, Lang CA. Glutathione biosynthesis in the aging adult yellow-fever mosquito [Aedes aegypti (Louisville)] Biochem. J. 1983;210(2):289–295. doi: 10.1042/bj2100289. [DOI] [PMC free article] [PubMed] [Google Scholar]
41.Hazelton GA, Lang CA. Glutathione contents of tissues in the aging mouse. Biochem. J. 1980;188(1):25–30. doi: 10.1042/bj1880025. [DOI] [PMC free article] [PubMed] [Google Scholar]
42.Michels AJ, Joisher N, Hagen TM. Age-related decline of sodium-dependent ascorbic acid transport in isolated rat hepatocytes. Arch. Biochem. Biophys. 2003;410(1):112–120. doi: 10.1016/s0003-9861(02)00678-1. [DOI] [PubMed] [Google Scholar]
43.Svensson L, Wu C, Hulthe P, Johannessen K, Engel JA. Effect of ageing on extracellular ascorbate concentration in rat brain. Brain Res. 1993;609(1–2):36–40. doi: 10.1016/0006-8993(93)90851-d. [DOI] [PubMed] [Google Scholar]
44.Sahoo A, Chainy GB. Alterations in the activities of cerebral antioxidant enzymes of rat are related to aging. Int. J. Dev. Neurosci. 1997;15(8):939–948. doi: 10.1016/s0736-5748(97)00049-x. [DOI] [PubMed] [Google Scholar]
45.Rikans LE, Moore DR. Effect of aging on aqueous-phase antioxidants in tissues of male Fischer rats. Biochim. Biophys. Acta. 1988;966(3):269–275. doi: 10.1016/0304-4165(88)90076-1. [DOI] [PubMed] [Google Scholar]
46.Jose da Rocha A, Tulio Braga F, Carlos Martins Maia A, Jr, Jorge da Silva C, Toyama C, Pereira Pinto Gama H, Kok F, Rodrigues Gomes H. Lactate detection by MRS in mitochondrial encephalopathy: optimization of technical parameters. J. Neuroimaging. 2008;18(1):1–8. doi: 10.1111/j.1552-6569.2007.00205.x. [DOI] [PubMed] [Google Scholar]
47.Lin DD, Crawford TO, Barker PB. Proton MR spectroscopy in the diagnostic evaluation of suspected mitochondrial disease. Am. J. Neuroradiol. 2003;24(1):33–41. [PMC free article] [PubMed] [Google Scholar]
48.Chang L, Ernst T, Poland RE, Jenden DJ. In vivo proton magnetic resonance spectroscopy of the normal aging human brain. Life Sci. 1996;58(22):2049–2056. doi: 10.1016/0024-3205(96)00197-x. [DOI] [PubMed] [Google Scholar]
49.Brooks JC, Roberts N, Kemp GJ, Gosney MA, Lye M, Whitehouse GH. A proton magnetic resonance spectroscopy study of age-related changes in frontal lobe metabolite concentrations. Cereb. Cortex. 2001;11(7):598–605. doi: 10.1093/cercor/11.7.598. [DOI] [PubMed] [Google Scholar]
50.Peters A. The effects of normal aging on myelin and nerve fibers: a review. J. Neurocytol. 2002;31(8–9):581–593. doi: 10.1023/a:1025731309829. [DOI] [PubMed] [Google Scholar]
51.Dickstein DL, Kabaso D, Rocher AB, Luebke JI, Wearne SL, Hof PR. Changes in the structural complexity of the aged brain. Aging Cell. 2007;6(3):275–284. doi: 10.1111/j.1474-9726.2007.00289.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
52.Kirov II, Fleysher L, Fleysher R, Patil V, Liu S, Gonen O. Age dependence of regional proton metabolites T2 relaxation times in the human brain at 3 T. Magn. Reson. Med. 2008;60(4):790–795. doi: 10.1002/mrm.21715. [DOI] [PMC free article] [PubMed] [Google Scholar]
53.Schenker C, Meier D, Wichmann W, Boesiger P, Valavanis A. Age distribution and iron dependency of the T2 relaxation time in the globus pallidus and putamen. Neuroradiology. 1993;35(2):119–124. doi: 10.1007/BF00593967. [DOI] [PubMed] [Google Scholar]
54.Kaiser LG, Young K, Meyerhoff DJ, Mueller SG, Matson GB. A detailed analysis of localized J-difference GABA editing: theoretical and experimental study at 4 T. NMR Biomed. 2008;21(1):22–32. doi: 10.1002/nbm.1150. [DOI] [PubMed] [Google Scholar]
55.Edden RA, Barker PB. Spatial effects in the detection of gamma-aminobutyric acid: improved sensitivity at high fields using inner volume saturation. Magn. Reson. Med. 2007;58(6):1276–1282. doi: 10.1002/mrm.21383. [DOI] [PubMed] [Google Scholar]
56.Yablonskiy DA, Neil JJ, Raichle ME, Ackerman JJ. Homonuclear J coupling effects in volume localized NMR spectroscopy: pitfalls and solutions. Magn. Reson. Med. 1998;39(2):169–178. doi: 10.1002/mrm.1910390202. [DOI] [PubMed] [Google Scholar]
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