Microglia, the major population of brain resident macrophages, differentiate from yolk sac progenitors in the embryo and play multiple nonimmune roles in brain organization throughout development and life. Various microglia subtypes have been described by transcriptomic and proteomic signatures, involved metabolic pathways, morphology, intracellular complexity, time of residency, and ontogeny, both in development and in disease settings. Such macrophage heterogeneity increases with aging or neurodegeneration. Monocytes' infiltration and differentiation into monocyte-derived macrophages (MDMs) in the brain contribute to this diversity. Microbiota's role in brain diseases has been recently highlighted, revealing how microbial signals, such as metabolites, influence microglia and MDMs. In this brief review, we describe how these signals can influence microglia through their sensome and shape MDMs from their development in the bone marrow to their differentiation in the brain. Monocytes could then be a crucial player in the constitution of a dysbiotic gut-brain axis in neurodegenerative diseases and aging.
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http://dx.doi.org/10.1093/jimmun/vkae034 | DOI Listing |
J Immunol
March 2025
INSERM U1015, Gustave Roussy Cancer Campus, 114 rue Edouard Vaillant, Villejuif, 94805, France.
Microglia, the major population of brain resident macrophages, differentiate from yolk sac progenitors in the embryo and play multiple nonimmune roles in brain organization throughout development and life. Various microglia subtypes have been described by transcriptomic and proteomic signatures, involved metabolic pathways, morphology, intracellular complexity, time of residency, and ontogeny, both in development and in disease settings. Such macrophage heterogeneity increases with aging or neurodegeneration.
View Article and Find Full Text PDFGeroscience
March 2025
Dept. Of Bioinformatics, Semmelweis University, 1094, Budapest, Hungary.
The link between abnormal sleep duration and stroke outcomes remains contentious. This meta-analysis quantifies how both short and long sleep durations impact stroke incidence and mortality. A comprehensive search was conducted in PubMed, Web of Science, Cochrane Library, Embase, and Google Scholar up to November 1, 2024, to identify cohort studies evaluating sleep duration and stroke outcomes.
View Article and Find Full Text PDFGeroscience
March 2025
Doctoral College, Health Sciences Program, Semmelweis University, Budapest, Hungary.
Sleep duration is a crucial factor influencing health outcomes, yet its relationship with mortality remains debated. In this meta-analysis, we aimed to investigate the association between short and long sleep duration and all-cause mortality in adults, including sex-specific differences. A systematic search was performed in multiple databases, including PubMed, Cochrane Central, and Web of Science, up to October 2024.
View Article and Find Full Text PDFAdv Biol (Weinh)
March 2025
Medizinisches Proteom-Center, Medical Faculty, Ruhr-University Bochum, 44801, Bochum, Germany.
Aging is a progressive and irreversible process, serving as the primary risk factor for neurodegenerative disorders. This study aims to identify the molecular mechanisms underlying physiological aging within the substantia nigra, which is primarily affected by Parkinson's disease, and to draw potential conclusions on the earliest events leading to neurodegeneration in this specific brain region. The characterization of essential stages in aging progress can enhance knowledge of the mechanisms that promote the development of Parkinson's disease.
View Article and Find Full Text PDFACS Chem Neurosci
March 2025
Department of Chemistry and Biochemistry, University of Denver, F.W. Olin Hall, 2190 E Iliff Ave, Denver, Colorado 80210, United States.
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is the leading cause of dementia, affecting nearly 55 million people across the world. One of the central pathological factors associated with AD is the aggregation of Aβ, a peptide product cleaved through pathological processes in AD. Under pathological conditions, Aβ aggregates into insoluble plaques in the brain and impairs the function of neurons, which contributes to the cognitive decline associated with AD.
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