Microglia are the resident immune cells in the central nervous system and are constantly monitoring their environment. After an insult, they are activated and secrete both pro- and anti-inflammatory mediators. Thus, they can have both detrimental and protective actions. Microglia are activated in many conditions that involve chronic inflammation such as Alzheimer's and Parkinson's diseases and in neuropathic pain. Following cerebral ischemia and stroke, microglia are activated and acutely contribute to neuronal loss and infarct damage. Chronically, in this condition, neuroprotective actions of activated microglia include clearance of the dead cells and secretion of neurotrophins. Of great interest is the recent observation that following myocardial infarction, there is increased inflammation within the hypothalamus and a marked increase in activated microglia.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.biocel.2010.07.005 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Microglia modulate their cell state in response to various stimuli. Changes to cellular lipids often accompany shifts in microglial cell state, but the functional significance of these metabolic changes remains poorly understood. In human induced pluripotent stem cell-derived microglia, we observed that both extrinsic activation (by lipopolysaccharide treatment) and intrinsic triggers (the Alzheimer's disease-associated genotype) result in accumulation of triglyceride-rich lipid droplets.
View Article and Find Full Text PDFUnlabelled: Multiple sclerosis (MS) is an immune-mediated demyelinating disease of the central nervous system (CNS). Clemastine fumarate, the over-the-counter antihistamine and muscarinic receptor blocker, has remyelinating potential in MS. A clemastine arm was added to an ongoing platform clinical trial TRAP-MS ( NCT03109288 ) to identify a cerebrospinal fluid (CSF) remyelination signature and to collect safety data on clemastine in patients progressing independently of relapse activity (PIRA).
View Article and Find Full Text PDFNeuroprotective Effects of Eugenol Acetate Against Ischemic Stroke.
J Inflamm Res
January 2025
Department of Neurology, Nanjing Drum Tower Hospital, Clinical College of Nanjing University of Chinese Medicine, Nanjing, 210008, People's Republic of China.
Objective: To explore the neuroprotective effect of Eugenol Acetate (EA) on post-stroke neuroinflammation and investigate the underlying mechanisms.
Methods: For in vitro experiments, primary microglia were pre-incubated with EA for 2 hours, followed by lipopolysaccharide (LPS) stimulation for 24 hours or Oxygen-Glucose Deprivation (OGD) treatment for 4 hours. Real-time quantitative PCR, enzyme-linked immunosorbent assay (ELISA) and Western blot were performed to examine the expression levels of inflammatory cytokines in primary microglia.
C3/C3aR Bridges Spinal Astrocyte-Microglia Crosstalk and Accelerates Neuroinflammation in Morphine-Tolerant Rats.
CNS Neurosci Ther
January 2025
Department of Anesthesiology and Pain Medicine, Hubei Key Laboratory of Geriatric Anesthesia and Perioperative Brain Health, and Wuhan Clinical Research Center for Geriatric Anesthesia, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Aims: Communication within glial cells acts as a pivotal intermediary factor in modulating neuroimmune pathology. Meanwhile, an increasing awareness has emerged regarding the detrimental role of glial cells and neuroinflammation in morphine tolerance (MT). This study investigated the influence of crosstalk between astrocyte and microglia on the evolution of morphine tolerance.
View Article and Find Full Text PDFTREM2 affects DAM-like cell transformation in the acute phase of TBI in mice by regulating microglial glycolysis.
J Neuroinflammation
January 2025
Department of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Background: Traumatic brain injury (TBI) is characterized by high mortality and disability rates. Disease-associated microglia (DAM) are a newly discovered subtype of microglia. However, their presence and function in the acute phase of TBI remain unclear.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!