98%
921
2 minutes
20
Microglia are specialized immune cells that reside in the central nervous system (CNS) and play a crucial role in maintaining the homeostasis of the brain microenvironment. While traditionally regarded as a part of the innate immune system, recent research has highlighted their role in adaptive immunity. The CNS is no longer considered an immune-privileged organ, and increasing evidence suggests bidirectional communication between the immune system and the CNS. Microglia are sensitive to systemic immune signals and can respond to systemic inflammation by producing various inflammatory cytokines and chemokines. This response is mediated by activating pattern recognition receptors (PRRs), which recognize pathogen- and danger-associated molecular patterns in the systemic circulation. The microglial response to systemic inflammation has been implicated in several neurological conditions, including depression, anxiety, and cognitive impairment. Understanding the complex interplay between microglia and systemic immunity is crucial for developing therapeutic interventions to modulate immune responses in the CNS.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/978-3-031-55529-9_16 | DOI Listing |
Mol Biol Rep
September 2025
Department of Pharmacology, Govt. College of Pharmacy, Rohru, Shimla, Himachal Pradesh, 171207, India.
Alzheimer's disease (AD) is the most common, complex, and untreatable form of dementia which is characterized by severe cognitive, motor, neuropsychiatric, and behavioural impairments. These symptoms severely reduce the quality of life for patients and impose a significant burden on caregivers. The existing therapies offer only symptomatic relief without addressing the underlying silent pathological progression.
View Article and Find Full Text PDFAm J Respir Cell Mol Biol
September 2025
University of Toronto, Interdepartmental Division of Critical Care Medicine, Toronto, Ontario, Canada.
Post-Intensive Care Syndrome (PICS) is a serious condition involving physical weakness, depression, and cognitive impairment that develop during or after an intensive care unit (ICU) stay, often resulting in long-term declines in quality of life. Patients with acute respiratory distress syndrome (ARDS) and severe COVID-19 are at particularly high risk, yet the molecular mechanisms underlying PICS remain poorly understood. Here, we identify impaired Apelin-APJ signaling as a potential contributor to PICS pathogenesis via disruption of inter-organ homeostasis.
View Article and Find Full Text PDFBiomed Pharmacother
September 2025
Department of Medical Biochemistry, Molecular Biology, and Immunology, School of Medicine, University of Seville, Spain; Instituto de Biomedicina de Sevilla, IBiS/Hospital Universitario Virgen del Rocio/CSIC/Universidad de Sevilla, Seville, 41013, Spain. Electronic address:
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive impairment, synaptic dysfunction, and neuronal loss. Neuroinflammation, driven by the activation of microglia and astrocytes, is a key contributor to AD pathology, amplifying oxidative stress and amyloid-β toxicity. Modulation of neuroinflammatory pathways thus represents a promising therapeutic strategy.
View Article and Find Full Text PDFArch Med Res
September 2025
Universidad Autónoma de Nuevo León, College of Medicine, Biochemistry and Molecular Medicine Department, Monterrey, Mexico; Universidad Autónoma de Nuevo León, Center for Research and Development in Health Sciences, Neurometabolism Unit, Monterrey, Mexico. Electronic address:
Background: Long-chain ceramides have been implicated in anxiety-like behavior and in priming microglial activation, suggesting a possible lipid-immune crosstalk in emotional regulation.
Methods: We systemically administered a mixture of C16:0, C18:0, C22:0, C24:0, and C24:1 ceramides to adult male and female mice. Anxiety-like behavior was assessed with behavioral tests.
Front Immunol
September 2025
Department of Pharmacy, Shenzhen Longhua District Central Hospital, Shenzhen, China.
The immune interactions within the gut-brain axis represent a critical etiological factor in psychiatric disorders. The gut microbiota and their metabolites serve as biological mediators that regulate neuroimmune activation and suppression in the central nervous system (CNS). During intestinal immune activation, pro-inflammatory cytokines (, IL-6, TNF-α) propagate to the CNS compromised blood-brain barrier (BBB) integrity or vagal afferent fibers, disrupting neurotransmitter metabolism and inducing microglial hyperactivation, thereby exacerbating neuroinflammation.
View Article and Find Full Text PDF