Multiple sclerosis (MS) is a common autoimmune disease that primarily affects young adults. In this condition, the immune system attacks the myelin sheath of nerve cells, leading to a variety of neurological symptoms.

Background/Objectives: Vitamin B12 deficiency affects up to 40% of certain populations worldwide and has been associated with cardiometabolic risk. However, its relationship with detailed lipoprotein subfractions remains poorly defined. This study aimed to investigate the association between serum vitamin B12 levels and atherogenic lipid profiles using NMR-based lipoprotein subfraction analysis. Methods: In this retrospective cross-sectional study, data from 20,665 apparently healthy adults undergoing routine health screening were analyzed. Participants were categorized into quartiles based on serum vitamin B12 levels (Q1: ≤328 pg/mL; Q4: ≥540 pg/mL). Lipoprotein subfractions were quantified using Bruker NMR spectroscopy. The Atherogenic Index of Plasma was calculated as log₁₀(triglycerides/HDL-cholesterol). Statistical analyses included ANCOVA adjusted for age, with corrections for multiple comparisons. Results: Higher serum B12 levels were significantly associated with a more favorable lipid profile. Specifically, AIP values decreased progressively across B12 quartiles (Q1: −0.051 ± 0.273; Q4: −0.170 ± 0.294; p < 0.001, partial η² = 0.017). HDL-cholesterol increased (p < 0.001, partial η² = 0.008), while triglycerides and VLDL-TG subfractions (VLDL1-TG: p < 0.001; VLDL5-TG: p = 0.029) declined with higher B12 levels. Among LDL subfractions, small dense LDL (LDL5-TG) exhibited a consistent inverse association with B12 (p = 0.002, partial η² = 0.001). These associations were robust across all age strata, with no significant interaction between B12 levels and age. Conclusions: Serum vitamin B12 levels are inversely associated with atherogenic lipid parameters in a large cohort of asymptomatic individuals. Higher B12 status correlates with lower AIP, reduced triglyceride-rich lipoproteins, and diminished small dense LDL particles across all age groups. These findings suggest that B12 status may serve as a potential biomarker in cardiovascular risk assessment and highlight the need for prospective interventional studies.

Alzheimer’s disease (AD), a neurodegenerative, irreversible, and progressive brain disorder, is characterized by memory loss and cognitive dysfunction. In neurodegeneration, gut microbiota and their metabolites have an impact on behavior and brain function. This study aimed to identify fecal candidate discriminant metabolites in 5XFAD mice assosciated with AD as compared to an age-matched wild-type (WT) healthy mice groups at three different time points (3, 6, and 9 month) using Proton Nuclear Magnetic Resonance (¹H NMR) spectroscopy. A total of 18 male mice (n = 9 for 5XFAD mice and n = 9 for WT, with three animals per age group) were used to determine the fecal candidate discriminant metabolites. As a result of the study, it was identified a total of 67 metabolites in fecal samples. Among these, 19 metabolites were found significantly up-regulated or down-regulated in 5XFAD mice compared to WT mice during the disease progress. According to the volcano plot analysis (FC ≥ 1.2 and p-value ≤ 0.05), the potential candidate discriminant metabolites were fumarate and malate in 3-month-old 5XFAD mice, 3-methylxanthine, glucose, cholate, phenylacetate, and trimethylamine N-oxide (TMAO) in 6-month-old 5XFAD mice and cholate and succinate in 9-month-old 5XFAD mice. These findings highlight the potential of fecal metabolomics as a non-invasive exploratory approach for understanding AD disease mechanisms and progression. Furthermore, to the best of our knowledge, this pilot study is the first to utilize NMR spectroscopy to investigate age-stratified cross-sectional changes in fecal metabolites in 5xFAD mice, thereby advancing our understanding of disease progression and potentially informing future therapeutic strategies. Graphical Abstract The alternative text for this image may have been generated using AI.

Gastric cancer is one of the leading causes of cancer-related deaths worldwide, and due to its late-stage diagnosis, the prognosis is poor. Therefore, researching biomarkers that can be used in early diagnosis and prognostic processes is crucial. Insulin-like growth factor (IGF) signaling pathways play critical roles in cellular proliferation, apoptosis, differentiation, and tumor progression. This study investigated the biomarker potential of IGF-1, IGFBP-4, IGFBP-5, and PAPP-A in gastric cancer. Forty gastric cancer patients and forty healthy individuals were included, and protein levels in serum samples were measured using the ELISA method. The findings showed that IGF-1 levels were significantly decreased in the gastric cancer group, while IGFBP-4 levels were significantly increased. IGFBP-5 levels were also lower in gastric cancer patients. In contrast, PAPP-A levels did not differ significantly between the two groups. ROC analyses revealed that IGF-1, IGFBP-4, and IGFBP-5 have good discriminatory properties in the diagnosis of gastric cancer, while PAPP-A offers low diagnostic value. In conclusion, this study suggests that IGF pathway components, particularly IGF-1, IGFBP-4, and IGFBP-5, might be promising biomarker candidates for gastric cancer.

Background/Objectives: Triglyceride (TG), Total Cholesterol (TC), HDL cholesterol (HDL-C), and LDL cholesterol (LDL-C) levels are commonly tested routine lipid profiles (RLPs) for assessing cardiovascular disease (CVD) risk. While lipid levels are typically measured by using standard clinical chemistry tests in routine practice, Nuclear Magnetic Resonance (NMR) spectroscopy has recently been explored for its ability to determine lipid levels under clinical settings. This study aims to compare RLP and NMR analysis using 17,337 fresh serum samples. Additionally, it investigates the impacts of freezing–thawing on these parameters in 9559 frozen samples. Methods: RLP was performed by employing the Siemens Dimension clinical chemistry system. Furthermore, the lipid contents of the fresh and frozen serum samples were evaluated across different concentration ranges. Results: Lipid parameters of fresh samples ascertained with RLP and NMR were strongly correlated (r ≥ 0.93). Analysis with frozen samples revealed that the correlation between lipid measurements decreased below r ≤ 0.86, except for TG (r = 0.97). Additionally, at different concentration ranges, the lower-level ranges for all lipid parameters in both fresh and frozen samples exhibited weaker correlations. Conclusions: This study demonstrates that NMR spectroscopy is a reliable, rapid, chemical-free method for lipid analysis in fresh samples. However, in frozen samples, relying on NMR to support RLP offers a less reliable approach for lipid measurement.

Whether gut and brain molecular states covary within individual animals, rather than merely co-occurring at the group level, has rarely been tested in Alzheimer’s disease models. We profiled the hippocampus, cortex, cerebellum, intestine and feces of 18 male 5xFAD (5 familial AD mutations) (B6SJL background) mice and wild-type littermates at 3, 6 and 9 months by label-free proteomics, and feces additionally by shotgun metagenomics. The hippocampal proteome reproduced the amyloid-associated signature (App, Apoe, Hexb, Clu, Gfap), and protein-set analysis showed elevated microglial, lysosomal, astrocytic and endoplasmic reticulum chaperone proteins in the hippocampus and cortex, with no detectable difference in synaptic or mitochondrial sets. Fecal Shannon diversity was reduced, and the bile-acid-modifying genera Romboutsia and Turicibacter were nearly absent in all 5xFAD animals from 3 months (cage nested within genotype). Multi-omics factor analysis recovered a genotype-associated factor shared across brain and gut views (exact permutation p = 0.00125) that explained at most 6.3% of variance in any view and was preprocessing-dependent. After removal of group structure, correlation burden did not exceed a within-cell permutation null, and neither did same-animal positive controls. The 5xFAD genotype thus alters every compartment examined, and a modest latent structure links them; because the design excludes only strong or dense individual-level coupling, the null result bounds design resolution rather than showing that gut and brain are uncoupled.