Related Experiment Video

Updated: Jun 10, 2026

Improved 3D Hydrogel Cultures of Primary Glial Cells for In Vitro Modelling of Neuroinflammation
09:19

Improved 3D Hydrogel Cultures of Primary Glial Cells for In Vitro Modelling of Neuroinflammation

Published on: December 8, 2017

Contribution of systemic inflammation to chronic neurodegeneration

V Hugh Perry1

  • 1School of Biological Sciences, University of Southampton, Southampton General Hospital, Southampton SO16 6YD, UK. vhp@soton.ac.uk

Acta Neuropathologica
|July 21, 2010
PubMed

Insights

Systemic inflammation can worsen neurodegenerative diseases by activating brain immune cells called microglia. Targeting these pathways may slow disease progression and improve patient quality of life.

Area of Science:

  • Neuroimmunology
  • Neuroinflammation
  • Brain-Body Communication

Background:

  • Systemic infections and inflammation trigger sickness behavior via brain signaling.
  • Microglia, the brain's immune cells, are crucial in this communication.
  • In aged or diseased brains, microglia adopt a primed, more reactive state.

Purpose of the Study:

  • To investigate how systemic inflammation affects primed microglia in the brain.
  • To explore the role of microglia in the exacerbation of neurodegenerative diseases.
  • To identify therapeutic targets for managing neuroinflammation in chronic conditions.

Main Methods:

  • The study reviews recent evidence on microglia activation by systemic inflammation.
  • It examines the shift from homeostatic to maladaptive microglial responses.
  • Focuses on signaling pathways from the periphery to the brain.

Main Results:

  • Systemic inflammation can switch primed microglia to an aggressive phenotype.
  • This leads to enhanced production of pro-inflammatory mediators.
  • Aggravated neuroinflammation may accelerate neurodegenerative disease progression.

Conclusions:

  • The maladaptive role of microglia in aged/diseased brains presents a therapeutic target.
  • Treating systemic inflammation or blocking peripheral-to-brain signaling may mitigate neurodegeneration.
  • Interventions could improve quality of life for patients with chronic neurodegenerative diseases.

More Related Videos

Isolating Central Nervous System Tissues and Associated Meninges for the Downstream Analysis of Immune cells09:35

Isolating Central Nervous System Tissues and Associated Meninges for the Downstream Analysis of Immune cells

Published on: May 19, 2020

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates09:12

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

Published on: January 30, 2014

Related Concept Videos

Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
Inflammation01:38

Inflammation

Overview
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...
Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...