Related Experiment Video

Updated: May 6, 2026

Detecting Amyloid-β Accumulation via Immunofluorescent Staining in a Mouse Model of Alzheimer's Disease
08:25

Detecting Amyloid-β Accumulation via Immunofluorescent Staining in a Mouse Model of Alzheimer's Disease

Published on: April 19, 2021

2.4K

Sustained Alzheimer's amyloid pathology in myeloid differentiation protein-88-deficient APPswe/PS1 mice

Y Goll1, U Bekenstein, S Barbash

  • 1Department of Biological Chemistry and the Edmond and Lily Safra Center of Brain Science, The Hebrew University of Jerusalem, Jerusalem, Israel.

Neuro-Degenerative Diseases
|November 7, 2013
PubMed
Abstract

Insights

Innate immune system activation, regulated by the myeloid differentiation protein 88 (MyD88) pathway, may influence Alzheimer's disease (AD) pathology. Impaired innate immunity was linked to reduced lifespan in AD mouse models.

Area of Science:

  • Neuroscience
  • Immunology
  • Genetics

Background:

  • Alzheimer's disease (AD) pathogenesis involves sporadic cases potentially linked to innate immune activation.
  • Microglial Toll-like receptors (TLRs) and the myeloid differentiation protein 88 (MyD88) pathway are key regulators of this immune response.

Purpose of the Study:

  • To investigate the role of innate immunity in Alzheimer's disease pathology.
  • To determine the impact of MyD88 pathway deficiency on AD progression in a mouse model.

Main Methods:

  • APPsw/PS1ΔE9 transgenic mice were crossed with MyD88-deficient mice.
  • Analysis of amyloid-beta peptide levels, plaque density, and neuroinflammation markers in progeny.

Main Results:

  • No significant differences were observed in soluble amyloid-beta peptides, amyloid plaque density, or neuroimmune staining between groups.
  • Double-transgenic mice (APPsw/PS1ΔE9 and MyD88-deficient) exhibited a significantly reduced lifespan compared to controls.

Conclusions:

  • Impaired innate immune responses, specifically via the MyD88 pathway, may contribute to Alzheimer's disease pathology.
  • This study suggests a potential role for innate immunity in AD pathogenesis and disease progression.

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

7.6K
Imaging the Intracellular Trafficking of APP with Photoactivatable GFP07:55

Imaging the Intracellular Trafficking of APP with Photoactivatable GFP

Published on: October 17, 2015

10.7K

Related Concept Videos

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...
44
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,...
10.4K
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...
38