Related Experiment Video

Updated: Aug 9, 2026

Correlative Light and Electron Microscopy to Study Microglial Interactions with β-Amyloid Plaques
10:52

Correlative Light and Electron Microscopy to Study Microglial Interactions with β-Amyloid Plaques

Published on: June 1, 2016

Microglial interaction with beta-amyloid: implications for the pathogenesis of Alzheimer's disease

M E Bamberger1, G E Landreth

  • 1Alzheimer Research Laboratory, Department of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA.

Microscopy Research and Technique
|July 17, 2001
PubMed

Insights

Alzheimer's disease (AD) involves brain inflammation driven by activated microglia responding to amyloid plaques. Inhibiting this microglial inflammation may offer new therapeutic strategies for AD.

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Alzheimer's disease (AD) is characterized by significant neuroinflammation.
  • Elevated levels of proinflammatory molecules are present in the AD brain.
  • Activated microglia cluster around senile plaques in AD patients.

Purpose of the Study:

  • To investigate the role of microglial activation in Alzheimer's disease pathogenesis.
  • To explore the inflammatory mechanisms underlying neuronal toxicity in AD.
  • To identify potential therapeutic targets for AD by focusing on neuroinflammation.

Main Methods:

  • Analysis of proinflammatory molecules in the AD brain.
  • Observation of microglial activation and clustering in relation to amyloid plaques.
  • Review of studies on non-steroidal anti-inflammatory drug (NSAID) treatment in AD patients.
  • Examination of microglial response to beta-amyloid (Abeta) deposition and signaling pathways.

Main Results:

  • Activated microglia produce proinflammatory molecules and reactive oxygen/nitrogen species.
  • Microglial activation is triggered by fibrillar Abeta interacting with cell surface receptors.
  • These inflammatory products contribute to neuronal toxicity and death.
  • NSAID treatment has been associated with reduced AD risk and delayed progression.

Conclusions:

  • Microglial-mediated inflammation is a key component in Alzheimer's disease etiology.
  • Targeting microglial inflammatory responses presents a promising therapeutic avenue for AD intervention.
  • Understanding microglial signaling pathways activated by Abeta is crucial for developing new treatments.

More Related Videos

Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease09:33

Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

Published on: December 26, 2016

Cell-based Assay to Study Antibody-mediated Tau Clearance by Microglia07:18

Cell-based Assay to Study Antibody-mediated Tau Clearance by Microglia

Published on: November 9, 2018

Related Concept Videos

Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining, normally used to...
Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
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...
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...