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GraphPad Software Inc tukey boxplots graphpad prism 10 software
Results of two‐way analysis of variance comparing the relative serum abundance of individual metabolites across four groups, stratified by treatment status and brain atrophy progression as determined from magnetic resonance imaging over the 2 year follow‐up period: placebo progressors (dark red, N = 31), placebo stable (light red, N = 31), B vitamin progressors (non‐responders; dark blue, N = 14), and B vitamin stable (responders; light blue, N = 51). The figure presents follow‐up metabolite levels (adjusted for baseline) to enable interpretation of comparisons across treatment arms (placebo vs. B vitamins), progression status (progressors vs. stable), and within‐group treatment response (responders vs. <t>non‐responders).Tukey</t> post hoc analysis was performed, with results summarized in Table in supporting information. Significant and marginal p values are displayed above the graphs; metabolites without displayed p values were not associated with any significant pairwise comparisons. A, α‐ketoglutaric acid (treatment p = 0.03; atrophy p = 0.32); (B) glutamic acid (treatment p = 0.06; atrophy p = 0.53); (C) succinic acid (treatment p = 0.03; atrophy p = 0.19); (D) glucose (treatment p = 0.12; atrophy p = 0.11); (E) malic acid (treatment p = 0.03; atrophy p = 0.48); (F) N ‐acetylglutamate (treatment p = 0.20; atrophy p = 0.51); (G) glutaric acid (treatment p = 0.10; atrophy p = 0.36); (H) lactic acid (treatment p = 0.06; atrophy p = 0.41); (I) pyruvic acid (treatment p = 0.17; atrophy p = 0.66); (J) α‐ketobutyric (treatment p = 0.03; atrophy p = 0.17); (K) quinolinic acid (treatment p = 0.04; atrophy p = 0.15); (L) glutamine (treatment effect p = 0.19; atrophy effect p = 0.38). One outlier was excluded from the graphical representation to enhance data clarity. This exclusion did not significantly impact the results. VB, vitamin B.
Tukey Boxplots Graphpad Prism 10 Software, supplied by GraphPad Software Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Role of B vitamins in modulating homocysteine and metabolic pathways linked to brain atrophy: Metabolomics insights from the VITACOG trial"

Article Title: Role of B vitamins in modulating homocysteine and metabolic pathways linked to brain atrophy: Metabolomics insights from the VITACOG trial

Journal: Alzheimer's & Dementia

doi: 10.1002/alz.70521

Results of two‐way analysis of variance comparing the relative serum abundance of individual metabolites across four groups, stratified by treatment status and brain atrophy progression as determined from magnetic resonance imaging over the 2 year follow‐up period: placebo progressors (dark red, N = 31), placebo stable (light red, N = 31), B vitamin progressors (non‐responders; dark blue, N = 14), and B vitamin stable (responders; light blue, N = 51). The figure presents follow‐up metabolite levels (adjusted for baseline) to enable interpretation of comparisons across treatment arms (placebo vs. B vitamins), progression status (progressors vs. stable), and within‐group treatment response (responders vs. non‐responders).Tukey post hoc analysis was performed, with results summarized in Table in supporting information. Significant and marginal p values are displayed above the graphs; metabolites without displayed p values were not associated with any significant pairwise comparisons. A, α‐ketoglutaric acid (treatment p = 0.03; atrophy p = 0.32); (B) glutamic acid (treatment p = 0.06; atrophy p = 0.53); (C) succinic acid (treatment p = 0.03; atrophy p = 0.19); (D) glucose (treatment p = 0.12; atrophy p = 0.11); (E) malic acid (treatment p = 0.03; atrophy p = 0.48); (F) N ‐acetylglutamate (treatment p = 0.20; atrophy p = 0.51); (G) glutaric acid (treatment p = 0.10; atrophy p = 0.36); (H) lactic acid (treatment p = 0.06; atrophy p = 0.41); (I) pyruvic acid (treatment p = 0.17; atrophy p = 0.66); (J) α‐ketobutyric (treatment p = 0.03; atrophy p = 0.17); (K) quinolinic acid (treatment p = 0.04; atrophy p = 0.15); (L) glutamine (treatment effect p = 0.19; atrophy effect p = 0.38). One outlier was excluded from the graphical representation to enhance data clarity. This exclusion did not significantly impact the results. VB, vitamin B.
Figure Legend Snippet: Results of two‐way analysis of variance comparing the relative serum abundance of individual metabolites across four groups, stratified by treatment status and brain atrophy progression as determined from magnetic resonance imaging over the 2 year follow‐up period: placebo progressors (dark red, N = 31), placebo stable (light red, N = 31), B vitamin progressors (non‐responders; dark blue, N = 14), and B vitamin stable (responders; light blue, N = 51). The figure presents follow‐up metabolite levels (adjusted for baseline) to enable interpretation of comparisons across treatment arms (placebo vs. B vitamins), progression status (progressors vs. stable), and within‐group treatment response (responders vs. non‐responders).Tukey post hoc analysis was performed, with results summarized in Table in supporting information. Significant and marginal p values are displayed above the graphs; metabolites without displayed p values were not associated with any significant pairwise comparisons. A, α‐ketoglutaric acid (treatment p = 0.03; atrophy p = 0.32); (B) glutamic acid (treatment p = 0.06; atrophy p = 0.53); (C) succinic acid (treatment p = 0.03; atrophy p = 0.19); (D) glucose (treatment p = 0.12; atrophy p = 0.11); (E) malic acid (treatment p = 0.03; atrophy p = 0.48); (F) N ‐acetylglutamate (treatment p = 0.20; atrophy p = 0.51); (G) glutaric acid (treatment p = 0.10; atrophy p = 0.36); (H) lactic acid (treatment p = 0.06; atrophy p = 0.41); (I) pyruvic acid (treatment p = 0.17; atrophy p = 0.66); (J) α‐ketobutyric (treatment p = 0.03; atrophy p = 0.17); (K) quinolinic acid (treatment p = 0.04; atrophy p = 0.15); (L) glutamine (treatment effect p = 0.19; atrophy effect p = 0.38). One outlier was excluded from the graphical representation to enhance data clarity. This exclusion did not significantly impact the results. VB, vitamin B.

Techniques Used: Magnetic Resonance Imaging



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Results of two‐way analysis of variance comparing the relative serum abundance of individual metabolites across four groups, stratified by treatment status and brain atrophy progression as determined from magnetic resonance imaging over the 2 year follow‐up period: placebo progressors (dark red, N = 31), placebo stable (light red, N = 31), B vitamin progressors (non‐responders; dark blue, N = 14), and B vitamin stable (responders; light blue, N = 51). The figure presents follow‐up metabolite levels (adjusted for baseline) to enable interpretation of comparisons across treatment arms (placebo vs. B vitamins), progression status (progressors vs. stable), and within‐group treatment response (responders vs. <t>non‐responders).Tukey</t> post hoc analysis was performed, with results summarized in Table in supporting information. Significant and marginal p values are displayed above the graphs; metabolites without displayed p values were not associated with any significant pairwise comparisons. A, α‐ketoglutaric acid (treatment p = 0.03; atrophy p = 0.32); (B) glutamic acid (treatment p = 0.06; atrophy p = 0.53); (C) succinic acid (treatment p = 0.03; atrophy p = 0.19); (D) glucose (treatment p = 0.12; atrophy p = 0.11); (E) malic acid (treatment p = 0.03; atrophy p = 0.48); (F) N ‐acetylglutamate (treatment p = 0.20; atrophy p = 0.51); (G) glutaric acid (treatment p = 0.10; atrophy p = 0.36); (H) lactic acid (treatment p = 0.06; atrophy p = 0.41); (I) pyruvic acid (treatment p = 0.17; atrophy p = 0.66); (J) α‐ketobutyric (treatment p = 0.03; atrophy p = 0.17); (K) quinolinic acid (treatment p = 0.04; atrophy p = 0.15); (L) glutamine (treatment effect p = 0.19; atrophy effect p = 0.38). One outlier was excluded from the graphical representation to enhance data clarity. This exclusion did not significantly impact the results. VB, vitamin B.
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Results of two‐way analysis of variance comparing the relative serum abundance of individual metabolites across four groups, stratified by treatment status and brain atrophy progression as determined from magnetic resonance imaging over the 2 year follow‐up period: placebo progressors (dark red, N = 31), placebo stable (light red, N = 31), B vitamin progressors (non‐responders; dark blue, N = 14), and B vitamin stable (responders; light blue, N = 51). The figure presents follow‐up metabolite levels (adjusted for baseline) to enable interpretation of comparisons across treatment arms (placebo vs. B vitamins), progression status (progressors vs. stable), and within‐group treatment response (responders vs. <t>non‐responders).Tukey</t> post hoc analysis was performed, with results summarized in Table in supporting information. Significant and marginal p values are displayed above the graphs; metabolites without displayed p values were not associated with any significant pairwise comparisons. A, α‐ketoglutaric acid (treatment p = 0.03; atrophy p = 0.32); (B) glutamic acid (treatment p = 0.06; atrophy p = 0.53); (C) succinic acid (treatment p = 0.03; atrophy p = 0.19); (D) glucose (treatment p = 0.12; atrophy p = 0.11); (E) malic acid (treatment p = 0.03; atrophy p = 0.48); (F) N ‐acetylglutamate (treatment p = 0.20; atrophy p = 0.51); (G) glutaric acid (treatment p = 0.10; atrophy p = 0.36); (H) lactic acid (treatment p = 0.06; atrophy p = 0.41); (I) pyruvic acid (treatment p = 0.17; atrophy p = 0.66); (J) α‐ketobutyric (treatment p = 0.03; atrophy p = 0.17); (K) quinolinic acid (treatment p = 0.04; atrophy p = 0.15); (L) glutamine (treatment effect p = 0.19; atrophy effect p = 0.38). One outlier was excluded from the graphical representation to enhance data clarity. This exclusion did not significantly impact the results. VB, vitamin B.
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Results of two‐way analysis of variance comparing the relative serum abundance of individual metabolites across four groups, stratified by treatment status and brain atrophy progression as determined from magnetic resonance imaging over the 2 year follow‐up period: placebo progressors (dark red, N = 31), placebo stable (light red, N = 31), B vitamin progressors (non‐responders; dark blue, N = 14), and B vitamin stable (responders; light blue, N = 51). The figure presents follow‐up metabolite levels (adjusted for baseline) to enable interpretation of comparisons across treatment arms (placebo vs. B vitamins), progression status (progressors vs. stable), and within‐group treatment response (responders vs. <t>non‐responders).Tukey</t> post hoc analysis was performed, with results summarized in Table in supporting information. Significant and marginal p values are displayed above the graphs; metabolites without displayed p values were not associated with any significant pairwise comparisons. A, α‐ketoglutaric acid (treatment p = 0.03; atrophy p = 0.32); (B) glutamic acid (treatment p = 0.06; atrophy p = 0.53); (C) succinic acid (treatment p = 0.03; atrophy p = 0.19); (D) glucose (treatment p = 0.12; atrophy p = 0.11); (E) malic acid (treatment p = 0.03; atrophy p = 0.48); (F) N ‐acetylglutamate (treatment p = 0.20; atrophy p = 0.51); (G) glutaric acid (treatment p = 0.10; atrophy p = 0.36); (H) lactic acid (treatment p = 0.06; atrophy p = 0.41); (I) pyruvic acid (treatment p = 0.17; atrophy p = 0.66); (J) α‐ketobutyric (treatment p = 0.03; atrophy p = 0.17); (K) quinolinic acid (treatment p = 0.04; atrophy p = 0.15); (L) glutamine (treatment effect p = 0.19; atrophy effect p = 0.38). One outlier was excluded from the graphical representation to enhance data clarity. This exclusion did not significantly impact the results. VB, vitamin B.
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Results of two‐way analysis of variance comparing the relative serum abundance of individual metabolites across four groups, stratified by treatment status and brain atrophy progression as determined from magnetic resonance imaging over the 2 year follow‐up period: placebo progressors (dark red, N = 31), placebo stable (light red, N = 31), B vitamin progressors (non‐responders; dark blue, N = 14), and B vitamin stable (responders; light blue, N = 51). The figure presents follow‐up metabolite levels (adjusted for baseline) to enable interpretation of comparisons across treatment arms (placebo vs. B vitamins), progression status (progressors vs. stable), and within‐group treatment response (responders vs. <t>non‐responders).Tukey</t> post hoc analysis was performed, with results summarized in Table in supporting information. Significant and marginal p values are displayed above the graphs; metabolites without displayed p values were not associated with any significant pairwise comparisons. A, α‐ketoglutaric acid (treatment p = 0.03; atrophy p = 0.32); (B) glutamic acid (treatment p = 0.06; atrophy p = 0.53); (C) succinic acid (treatment p = 0.03; atrophy p = 0.19); (D) glucose (treatment p = 0.12; atrophy p = 0.11); (E) malic acid (treatment p = 0.03; atrophy p = 0.48); (F) N ‐acetylglutamate (treatment p = 0.20; atrophy p = 0.51); (G) glutaric acid (treatment p = 0.10; atrophy p = 0.36); (H) lactic acid (treatment p = 0.06; atrophy p = 0.41); (I) pyruvic acid (treatment p = 0.17; atrophy p = 0.66); (J) α‐ketobutyric (treatment p = 0.03; atrophy p = 0.17); (K) quinolinic acid (treatment p = 0.04; atrophy p = 0.15); (L) glutamine (treatment effect p = 0.19; atrophy effect p = 0.38). One outlier was excluded from the graphical representation to enhance data clarity. This exclusion did not significantly impact the results. VB, vitamin B.
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Results of two‐way analysis of variance comparing the relative serum abundance of individual metabolites across four groups, stratified by treatment status and brain atrophy progression as determined from magnetic resonance imaging over the 2 year follow‐up period: placebo progressors (dark red, N = 31), placebo stable (light red, N = 31), B vitamin progressors (non‐responders; dark blue, N = 14), and B vitamin stable (responders; light blue, N = 51). The figure presents follow‐up metabolite levels (adjusted for baseline) to enable interpretation of comparisons across treatment arms (placebo vs. B vitamins), progression status (progressors vs. stable), and within‐group treatment response (responders vs. <t>non‐responders).Tukey</t> post hoc analysis was performed, with results summarized in Table in supporting information. Significant and marginal p values are displayed above the graphs; metabolites without displayed p values were not associated with any significant pairwise comparisons. A, α‐ketoglutaric acid (treatment p = 0.03; atrophy p = 0.32); (B) glutamic acid (treatment p = 0.06; atrophy p = 0.53); (C) succinic acid (treatment p = 0.03; atrophy p = 0.19); (D) glucose (treatment p = 0.12; atrophy p = 0.11); (E) malic acid (treatment p = 0.03; atrophy p = 0.48); (F) N ‐acetylglutamate (treatment p = 0.20; atrophy p = 0.51); (G) glutaric acid (treatment p = 0.10; atrophy p = 0.36); (H) lactic acid (treatment p = 0.06; atrophy p = 0.41); (I) pyruvic acid (treatment p = 0.17; atrophy p = 0.66); (J) α‐ketobutyric (treatment p = 0.03; atrophy p = 0.17); (K) quinolinic acid (treatment p = 0.04; atrophy p = 0.15); (L) glutamine (treatment effect p = 0.19; atrophy effect p = 0.38). One outlier was excluded from the graphical representation to enhance data clarity. This exclusion did not significantly impact the results. VB, vitamin B.
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Results of two‐way analysis of variance comparing the relative serum abundance of individual metabolites across four groups, stratified by treatment status and brain atrophy progression as determined from magnetic resonance imaging over the 2 year follow‐up period: placebo progressors (dark red, N = 31), placebo stable (light red, N = 31), B vitamin progressors (non‐responders; dark blue, N = 14), and B vitamin stable (responders; light blue, N = 51). The figure presents follow‐up metabolite levels (adjusted for baseline) to enable interpretation of comparisons across treatment arms (placebo vs. B vitamins), progression status (progressors vs. stable), and within‐group treatment response (responders vs. <t>non‐responders).Tukey</t> post hoc analysis was performed, with results summarized in Table in supporting information. Significant and marginal p values are displayed above the graphs; metabolites without displayed p values were not associated with any significant pairwise comparisons. A, α‐ketoglutaric acid (treatment p = 0.03; atrophy p = 0.32); (B) glutamic acid (treatment p = 0.06; atrophy p = 0.53); (C) succinic acid (treatment p = 0.03; atrophy p = 0.19); (D) glucose (treatment p = 0.12; atrophy p = 0.11); (E) malic acid (treatment p = 0.03; atrophy p = 0.48); (F) N ‐acetylglutamate (treatment p = 0.20; atrophy p = 0.51); (G) glutaric acid (treatment p = 0.10; atrophy p = 0.36); (H) lactic acid (treatment p = 0.06; atrophy p = 0.41); (I) pyruvic acid (treatment p = 0.17; atrophy p = 0.66); (J) α‐ketobutyric (treatment p = 0.03; atrophy p = 0.17); (K) quinolinic acid (treatment p = 0.04; atrophy p = 0.15); (L) glutamine (treatment effect p = 0.19; atrophy effect p = 0.38). One outlier was excluded from the graphical representation to enhance data clarity. This exclusion did not significantly impact the results. VB, vitamin B.
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Results of two‐way analysis of variance comparing the relative serum abundance of individual metabolites across four groups, stratified by treatment status and brain atrophy progression as determined from magnetic resonance imaging over the 2 year follow‐up period: placebo progressors (dark red, N = 31), placebo stable (light red, N = 31), B vitamin progressors (non‐responders; dark blue, N = 14), and B vitamin stable (responders; light blue, N = 51). The figure presents follow‐up metabolite levels (adjusted for baseline) to enable interpretation of comparisons across treatment arms (placebo vs. B vitamins), progression status (progressors vs. stable), and within‐group treatment response (responders vs. <t>non‐responders).Tukey</t> post hoc analysis was performed, with results summarized in Table in supporting information. Significant and marginal p values are displayed above the graphs; metabolites without displayed p values were not associated with any significant pairwise comparisons. A, α‐ketoglutaric acid (treatment p = 0.03; atrophy p = 0.32); (B) glutamic acid (treatment p = 0.06; atrophy p = 0.53); (C) succinic acid (treatment p = 0.03; atrophy p = 0.19); (D) glucose (treatment p = 0.12; atrophy p = 0.11); (E) malic acid (treatment p = 0.03; atrophy p = 0.48); (F) N ‐acetylglutamate (treatment p = 0.20; atrophy p = 0.51); (G) glutaric acid (treatment p = 0.10; atrophy p = 0.36); (H) lactic acid (treatment p = 0.06; atrophy p = 0.41); (I) pyruvic acid (treatment p = 0.17; atrophy p = 0.66); (J) α‐ketobutyric (treatment p = 0.03; atrophy p = 0.17); (K) quinolinic acid (treatment p = 0.04; atrophy p = 0.15); (L) glutamine (treatment effect p = 0.19; atrophy effect p = 0.38). One outlier was excluded from the graphical representation to enhance data clarity. This exclusion did not significantly impact the results. VB, vitamin B.
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Results of two‐way analysis of variance comparing the relative serum abundance of individual metabolites across four groups, stratified by treatment status and brain atrophy progression as determined from magnetic resonance imaging over the 2 year follow‐up period: placebo progressors (dark red, N = 31), placebo stable (light red, N = 31), B vitamin progressors (non‐responders; dark blue, N = 14), and B vitamin stable (responders; light blue, N = 51). The figure presents follow‐up metabolite levels (adjusted for baseline) to enable interpretation of comparisons across treatment arms (placebo vs. B vitamins), progression status (progressors vs. stable), and within‐group treatment response (responders vs. <t>non‐responders).Tukey</t> post hoc analysis was performed, with results summarized in Table in supporting information. Significant and marginal p values are displayed above the graphs; metabolites without displayed p values were not associated with any significant pairwise comparisons. A, α‐ketoglutaric acid (treatment p = 0.03; atrophy p = 0.32); (B) glutamic acid (treatment p = 0.06; atrophy p = 0.53); (C) succinic acid (treatment p = 0.03; atrophy p = 0.19); (D) glucose (treatment p = 0.12; atrophy p = 0.11); (E) malic acid (treatment p = 0.03; atrophy p = 0.48); (F) N ‐acetylglutamate (treatment p = 0.20; atrophy p = 0.51); (G) glutaric acid (treatment p = 0.10; atrophy p = 0.36); (H) lactic acid (treatment p = 0.06; atrophy p = 0.41); (I) pyruvic acid (treatment p = 0.17; atrophy p = 0.66); (J) α‐ketobutyric (treatment p = 0.03; atrophy p = 0.17); (K) quinolinic acid (treatment p = 0.04; atrophy p = 0.15); (L) glutamine (treatment effect p = 0.19; atrophy effect p = 0.38). One outlier was excluded from the graphical representation to enhance data clarity. This exclusion did not significantly impact the results. VB, vitamin B.
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Results of two‐way analysis of variance comparing the relative serum abundance of individual metabolites across four groups, stratified by treatment status and brain atrophy progression as determined from magnetic resonance imaging over the 2 year follow‐up period: placebo progressors (dark red, N = 31), placebo stable (light red, N = 31), B vitamin progressors (non‐responders; dark blue, N = 14), and B vitamin stable (responders; light blue, N = 51). The figure presents follow‐up metabolite levels (adjusted for baseline) to enable interpretation of comparisons across treatment arms (placebo vs. B vitamins), progression status (progressors vs. stable), and within‐group treatment response (responders vs. non‐responders).Tukey post hoc analysis was performed, with results summarized in Table in supporting information. Significant and marginal p values are displayed above the graphs; metabolites without displayed p values were not associated with any significant pairwise comparisons. A, α‐ketoglutaric acid (treatment p = 0.03; atrophy p = 0.32); (B) glutamic acid (treatment p = 0.06; atrophy p = 0.53); (C) succinic acid (treatment p = 0.03; atrophy p = 0.19); (D) glucose (treatment p = 0.12; atrophy p = 0.11); (E) malic acid (treatment p = 0.03; atrophy p = 0.48); (F) N ‐acetylglutamate (treatment p = 0.20; atrophy p = 0.51); (G) glutaric acid (treatment p = 0.10; atrophy p = 0.36); (H) lactic acid (treatment p = 0.06; atrophy p = 0.41); (I) pyruvic acid (treatment p = 0.17; atrophy p = 0.66); (J) α‐ketobutyric (treatment p = 0.03; atrophy p = 0.17); (K) quinolinic acid (treatment p = 0.04; atrophy p = 0.15); (L) glutamine (treatment effect p = 0.19; atrophy effect p = 0.38). One outlier was excluded from the graphical representation to enhance data clarity. This exclusion did not significantly impact the results. VB, vitamin B.

Journal: Alzheimer's & Dementia

Article Title: Role of B vitamins in modulating homocysteine and metabolic pathways linked to brain atrophy: Metabolomics insights from the VITACOG trial

doi: 10.1002/alz.70521

Figure Lengend Snippet: Results of two‐way analysis of variance comparing the relative serum abundance of individual metabolites across four groups, stratified by treatment status and brain atrophy progression as determined from magnetic resonance imaging over the 2 year follow‐up period: placebo progressors (dark red, N = 31), placebo stable (light red, N = 31), B vitamin progressors (non‐responders; dark blue, N = 14), and B vitamin stable (responders; light blue, N = 51). The figure presents follow‐up metabolite levels (adjusted for baseline) to enable interpretation of comparisons across treatment arms (placebo vs. B vitamins), progression status (progressors vs. stable), and within‐group treatment response (responders vs. non‐responders).Tukey post hoc analysis was performed, with results summarized in Table in supporting information. Significant and marginal p values are displayed above the graphs; metabolites without displayed p values were not associated with any significant pairwise comparisons. A, α‐ketoglutaric acid (treatment p = 0.03; atrophy p = 0.32); (B) glutamic acid (treatment p = 0.06; atrophy p = 0.53); (C) succinic acid (treatment p = 0.03; atrophy p = 0.19); (D) glucose (treatment p = 0.12; atrophy p = 0.11); (E) malic acid (treatment p = 0.03; atrophy p = 0.48); (F) N ‐acetylglutamate (treatment p = 0.20; atrophy p = 0.51); (G) glutaric acid (treatment p = 0.10; atrophy p = 0.36); (H) lactic acid (treatment p = 0.06; atrophy p = 0.41); (I) pyruvic acid (treatment p = 0.17; atrophy p = 0.66); (J) α‐ketobutyric (treatment p = 0.03; atrophy p = 0.17); (K) quinolinic acid (treatment p = 0.04; atrophy p = 0.15); (L) glutamine (treatment effect p = 0.19; atrophy effect p = 0.38). One outlier was excluded from the graphical representation to enhance data clarity. This exclusion did not significantly impact the results. VB, vitamin B.

Article Snippet: Quantitative data are shown as Tukey boxplots (GraphPad Prism 10 software), with whiskers extending to the furthest values within 1.5 times the interquartile range (IQR).

Techniques: Magnetic Resonance Imaging