Alzheimer's disease (AD) is a neurodegenerative disorder caused by a variety of factors, including age, genetic susceptibility, cardiovascular disease, traumatic brain injury, and environmental factors. The pathogenesis of AD is largely associated with the overproduction and accumulation of amyloid-β peptides and the hyperphosphorylation of tau protein in the brain. Recent studies have identified the presence of diverse pathogens, including viruses, bacteria, and parasites, in the tissues of AD patients, underscoring the critical role of central nervous system infections in inducing pathological changes associated with AD. Nevertheless, it remains unestablished about the specific mechanism by which infections lead to the occurrence of AD. As an important post-transcriptional RNA modification, RNA 5-methylcytosine (mC) methylation regulates a wide range of biological processes, including RNA splicing, nuclear export, stability, and translation, therefore affecting cellular function. Moreover, it has been recently demonstrated that multiple pathogenic microbial infections are associated with the mC methylation of the host. However, the role of mC methylation in infectious AD is still uncertain. Therefore, this review discusses the mechanisms of pathogen-induced AD and summarizes research on the molecular mechanisms of mC methylation in infectious AD, thereby providing new insight into exploring the mechanism underlying infectious AD.
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http://dx.doi.org/10.3389/fcell.2024.1440143 | DOI Listing |
Int J Surg
January 2025
Aging Research Center, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden.
Introduction: Lung function has been associated with cognitive decline and dementia, but the extent to which lung function impacts brain structural changes remains unclear. We aimed to investigate the association of lung function with structural macro- and micro-brain changes across mid- and late-life.
Methods: The study included a total of 37 164 neurologic disorder-free participants aged 40-70 years from the UK Biobank, who underwent brain MRI scans 9 years after baseline.
Neurochem Res
January 2025
Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder characterized by cognitive decline. Despite extensive research, therapeutic options remain limited. Varenicline, an αβ nicotinic acetylcholine receptor agonist, shows promise in enhancing cognitive function.
View Article and Find Full Text PDFHum Brain Mapp
February 2025
Department of Neurology, Washington University in St. Louis, St. Louis, Missouri, USA.
Neurodegeneration is presumed to be the pathological process measure most proximal to clinical symptom onset in Alzheimer Disease (AD). Structural MRI is routinely collected in research and clinical trial settings. Several quantitative MRI-based measures of atrophy have been proposed, but their low correspondence with each other has been previously documented.
View Article and Find Full Text PDFAlzheimers Dement
January 2025
Department of Pathology & Laboratory Medicine, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts, USA.
Alzheimers Dement
January 2025
Center for Motor Neuron Biology and Disease, Columbia University Medical Center, New York, New York, USA.
This proceedings article summarizes the inaugural "T Cells in the Brain" symposium held at Columbia University. Experts gathered to explore the role of T cells in neurodegenerative diseases. Key topics included characterization of antigen-specific immune responses, T cell receptor (TCR) repertoire, microbial etiology in Alzheimer's disease (AD), and microglia-T cell crosstalk, with a focus on how T cells affect neuroinflammation and AD biomarkers like amyloid beta and tau.
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