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Background: Vitamin B inadequacies and elevated homocysteine status have been associated with impaired cognitive and cardiometabolic health with aging. There is, however, a scarcity of research investigating integrated profiles of one-carbon (1C) metabolites in this context, including metabolites of interconnected folate, methionine, choline oxidation, and transsulfuration pathways.
Objectives: The study aimed to examine associations between vitamins B and 1C metabolites with cardiometabolic health and cognitive function in healthy older adults, including the interactive effects of Apolipoprotein E-ε4 status.
Methods: Three hundred and thirteen healthy participants (65-74 y, 65% female) were analyzed. Vitamins B were estimated according to dietary intake (4-d food records) and biochemical status (serum folate and vitamin B). Fasting plasma 1C metabolites were quantified by liquid chromatography with tandem mass spectrometry. Measures of cardiometabolic health included biochemical (lipid panel, blood glucose) and anthropometric markers. Cognitive function was assessed by the Computerized Mental Performance Assessment System (COMPASS) and Montreal Cognitive Assessment (MoCA). Associations were analyzed using multivariate linear (COMPASS, cardiometabolic health) and Poisson (MoCA) regression modeling.
Results: Over 90% of participants met dietary recommendations for riboflavin and vitamins B and B, but only 78% of males and 67% of females achieved adequate folate intakes. Higher serum folate and plasma betaine and glycine concentrations were associated with favorable cardiometabolic markers, whereas higher plasma choline and homocysteine concentrations were associated with greater cardiometabolic risk based on body mass index and serum lipids concentration values (P< 0.05). Vitamins B and homocysteine were not associated with cognitive performance in this cohort, though higher glycine concentrations were associated with better global cognitive performance (P = 0.017), episodic memory (P = 0.016), and spatial memory (P = 0.027) scores. Apolipoprotein E-ε4 status did not modify the relationship between vitamins B or 1C metabolites with cognitive function in linear regression analyses.
Conclusions: Vitamin B and 1C metabolite profiles showed divergent associations with cardiometabolic risk markers and limited associations with cognitive performance in this cohort of healthy older adults.
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http://dx.doi.org/10.1016/j.tjnut.2023.10.012 | DOI Listing |
Mol Nutr Food Res
September 2025
Department of Epidemiology and Health Statistics, School of Public Health, Qingdao University, Qingdao, China.
The relationship between dietary biotin intake and cognitive function remains unclear. This study explores the association between biotin and dementia, and the mediating role of inflammation indicators. Dietary biotin intake was assessed via the 24-h recall questionnaire.
View Article and Find Full Text PDFAmyotroph Lateral Scler Frontotemporal Degener
September 2025
Faculdade de Medicina, Centro de Estudos Egas Moniz, Universidade de Lisboa, Lisboa, Portugal.
This study aimed to derive standardized regression-based (SRB) reliable change indices (RCIs) for the cognitive section of the Portuguese Edinburgh Cognitive and Behavioral ALS Screen (ECAS-C). Forty-nine MND patients undergoing the ECAS were followed-up (T1) at 7.2 ± 2 months (range = 5-12).
View Article and Find Full Text PDFMol Psychiatry
September 2025
Institute of Neurology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Alzheimer's disease (AD), a leading cause of dementia, represents a critical unmet global medical need. While the precise mechanisms underlying AD pathogenesis remain elusive, increasing evidence underscores the pivotal role of neuroinflammation in driving cognitive impairment. N6-methyladenosine (m6A), an epigenetic modification regulating RNA metabolism, has been found to be dysregulated in AD.
View Article and Find Full Text PDFNeurosci Bull
September 2025
Zhejiang Key Laboratory of Organ Development and Regeneration, College of Life and Environmental Sciences, Hangzhou Normal University, Hangzhou, 311121, China.
The neurological manifestations of SHORT syndrome include intrauterine growth restriction, microcephaly, intellectual disability, hearing loss, and speech delay. SHORT syndrome is generally believed to be caused by PIK3R1 gene mutations and impaired PI3K-AKT activation. Recently, a clinical case report described a SHORT syndrome with a novel mutant in PRKCE gene encoding protein kinase Cε (PKCε).
View Article and Find Full Text PDFCognition
September 2025
Department of Psychological and Brain Sciences, University of Massachusetts Amherst, USA; Commonwealth Honors College, University of Massachusetts Amherst, USA. Electronic address: