Introduction: Blood biomarkers accurately identify Alzheimer's disease (AD) pathophysiology and axonal injury. We investigated the influence of food intake on AD-related biomarkers in cognitively healthy, obese adults at high metabolic risk.
Methods: One-hundred eleven participants underwent repeated blood sampling during 3 h after a standardized meal (postprandial group, PG). For comparison, blood was sampled from a fasting subgroup over 3 h (fasting group, FG). Plasma neurofilament light (NfL), glial fibrillary acidic protein (GFAP), amyloid-beta (Aβ) 42/40, phosphorylated tau (p-tau) 181 and 231, and total-tau were measured via single molecule array assays.
Results: Significant differences were found for NfL, GFAP, Aβ42/40, p-tau181, and p-tau231 between FG and PG. The greatest change to baseline occurred for GFAP and p-tau181 (120 min postprandially, p < 0.0001).
Conclusion: Our data suggest that AD-related biomarkers are altered by food intake. Further studies are needed to verify whether blood biomarker sampling should be performed in the fasting state.
Highlights: Acute food intake alters plasma biomarkers of Alzheimer's disease in obese, otherwise healthy adults. We also found dynamic fluctuations in plasma biomarkers concentration in the fasting state suggesting physiological diurnal variations. Further investigations are highly needed to verify if biomarker measurements should be performed in the fasting state and at a standardized time of day to improve the diagnostic accuracy.
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http://dx.doi.org/10.1002/alz.13163 | DOI Listing |
Methods Cell Biol
January 2025
Federal University of Santa Maria, Center for Natural and Exact Sciences, Department of Biochemistry and Molecular Biology, Graduate Program in Biological Sciences: Toxicological Biochemistry, Camobi, Santa Maria, RS, Brazil.
Alzheimer's disease (AD) is the leading cause of dementia in the elderly, clinically characterized by memory loss, cognitive decline, and behavioral disturbances. Its pathogenesis is not fully comprehended but involves intracellular depositions of amyloid beta peptide (Aβ) and neurofibrillary tangles of hyperphosphorylated tau. Currently, pharmacological interventions solely slow the progression of symptoms.
View Article and Find Full Text PDFMethods Cell Biol
January 2025
Department of Pharmacology, SPP School of Pharmacy & Technology Management, Mumbai, India. Electronic address:
The foremost cause of dementia is Alzheimer's disease (AD). The vital pathological hallmarks of AD are amyloid beta (Aβ) peptide and hyperphosphorylated tau (p-tau) protein. The current animal models used in AD research do not precisely replicate disease pathophysiology, making it difficult for researchers to quickly and effectively gather data or screen potential therapy possibilities.
View Article and Find Full Text PDFJ Prev Alzheimers Dis
February 2025
Department of Neurology, Fujian Medical University Union Hospital, Fujian Key Laboratory of Molecular Neurology and Institute of Neuroscience, Fujian Medical University, No.29, Xinquan Road, Gulou District, Fuzhou, Fujian Province, 350000, China; Institute of Clinical Neurology, Fujian Medical University, No.29 Xinquan Road, Gulou District, Fuzhou, Fujian Province, 350000, China. Electronic address:
Background: The effect of statins use on the incidence of Alzheimer's disease (AD) is still under debate, and it could be modified by a series of factors.
Objectives: We aimed to examine the association of statins use with the risk of cognitive impairment and AD, and assess the moderating roles of genetic susceptibility and other individual-related factors.
Design: A longitudinal study was conducted from the UK Biobank where individuals completed baseline surveys (2006-2010) and were followed (mean follow-up period: 9 years).
J Prev Alzheimers Dis
February 2025
Neurology, Fondazione IRCCS "San Gerardo dei Tintori", Monza, Italy; Milan Center for Neuroscience (NeuroMI), University of Milano-Bicocca, Monza, Italy; Laboratory of Neurobiology, School of Medicine and Surgery, University of Milano-Bicocca, Monza, Italy. Electronic address:
Background: The new criteria for Alzheimer's disease pave the way for the introduction of core blood biomarkers of Alzheimer's disease (BBAD) into clinical practice. However, this depends on the demonstration of sufficient accuracy and robustness of BBADs in the intended population.
Objectives: To assess the diagnostic performance of core BBADs in our memory clinic, comparing them with cerebrospinal fluid (CSF) analysis.
J Prev Alzheimers Dis
February 2025
Department of Biostatistics, Boston University School of Public Health, Boston, MA 02118, USA. Electronic address:
Background: Protein abundance levels, sensitive to both physiological changes and external interventions, are useful for assessing the Alzheimer's disease (AD) risk and treatment efficacy. However, identifying proteomic prognostic markers for AD is challenging by their high dimensionality and inherent correlations.
Methods: Our study analyzed 1128 plasma proteins, measured by the SOMAscan platform, from 858 participants 55 years and older (mean age 63 years, 52.
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