Related Experiment Video

Updated: Sep 10, 2026

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
09:12

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates

Published on: January 30, 2014

15.9K

Microglial Activation: Key Players in Sepsis-Associated Encephalopathy

Jiyun Hu1,2,3, Shucai Xie1,2,3, Haisong Zhang1,2,3

  • 1Department of Critical Care Medicine, Xiangya Hospital, Central South University, Changsha 410008, China.

Brain Sciences
|October 28, 2023
PubMed

Insights

Sepsis-associated encephalopathy (SAE) involves brain dysfunction and cognitive issues. Microglia activation, with M1/M2 states, plays a key role in SAE development and offers therapeutic targets.

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Sepsis-associated encephalopathy (SAE) is a frequent complication of sepsis, leading to significant cognitive deficits and mortality.
  • Microglia, the brain's resident immune cells, are implicated in SAE's pathophysiology.
  • Microglial activation involves distinct polarization states (M1/M2) affecting brain function.

Purpose of the Study:

  • To systematically review the pathogenesis, morphology, function, and phenotype of microglial activation in SAE.
  • To elucidate the relationship between microglial behavior and SAE occurrence, development, and cognitive impairment.
  • To outline potential therapeutic strategies targeting microglial phenotypes in SAE.

Main Methods:

  • Systematic review and description of existing literature on microglial activation in SAE.
  • Analysis of microglial morphology, gene expression, and functional changes.
  • Identification of therapeutic targets for modulating microglial responses.

Main Results:

  • Microglial activation is integral to the development and progression of SAE.
  • Distinct M1 and M2 microglial phenotypes are associated with SAE.
  • Microglial dysfunction correlates with cognitive impairments observed in SAE patients.

Conclusions:

  • Microglia are critically involved in SAE pathogenesis and associated cognitive sequelae.
  • Targeting microglial polarization offers a promising therapeutic avenue for SAE.
  • Modulating neuroinflammation toward beneficial microglial phenotypes may restore neurological function.
Keywords:
M1/M2 microglial polarizationcognitive impairmentmicroglial activationsepsis-associated encephalopathytherapeutic strategies

More Related Videos

Rapid and Refined CD11b Magnetic Isolation of Primary Microglia with Enhanced Purity and Versatility07:54

Rapid and Refined CD11b Magnetic Isolation of Primary Microglia with Enhanced Purity and Versatility

Published on: April 13, 2017

9.8K
Characterization and Isolation of Mouse Primary Microglia by Density Gradient Centrifugation10:21

Characterization and Isolation of Mouse Primary Microglia by Density Gradient Centrifugation

Published on: February 16, 2018

19.3K

Related Concept Videos

The Blood-brain Barrier00:49

The Blood-brain Barrier

Overview
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
Dementia l: Introduction01:22

Dementia l: Introduction

Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...