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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 microglia. Abnormal...

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Imaging the Intracellular Trafficking of APP with Photoactivatable GFP
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Aβ internalization by neurons and glia.

Amany Mohamed1, Elena Posse de Chaves

  • 1Department of Pharmacology, University of Alberta, Edmonton, AB, Canada T6G 2H7.

International Journal of Alzheimer'S Disease
|February 26, 2011
PubMed
Summary
This summary is machine-generated.

Intracellular amyloid beta accumulation is crucial in Alzheimer's disease pathogenesis. This study explores how amyloid beta enters neurons and its impact on neuronal health.

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Last Updated: Jun 4, 2026

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

Published on: June 1, 2016

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pathology

Background:

  • Amyloid beta (Aβ) peptides are found both inside and outside neurons in the brain.
  • The role of intracellular Aβ accumulation in Alzheimer's disease (AD) pathogenesis has been debated.
  • Emerging evidence highlights the significance of intraneuronal Aβ in AD development.

Purpose of the Study:

  • To review the molecular mechanisms of Aβ internalization into neurons.
  • To examine the relationship between Aβ uptake and neuronal dysfunction/death.
  • To briefly discuss Aβ uptake by glial cells.

Main Methods:

  • Literature review and synthesis of existing research on Aβ internalization.
  • Analysis of molecular pathways involved in Aβ uptake by neurons.
  • Examination of studies linking intraneuronal Aβ to neuronal pathology.

Main Results:

  • Intraneuronal Aβ can originate from intracellular amyloid precursor protein (APP) cleavage or extracellular Aβ uptake.
  • Specific molecular mechanisms facilitate Aβ internalization into neurons.
  • Neuronal Aβ internalization is linked to cellular dysfunction and neurodegeneration.

Conclusions:

  • Intracellular Aβ accumulation is a key factor in Alzheimer's disease.
  • Understanding Aβ internalization mechanisms is vital for targeting AD.
  • Further research into glial Aβ uptake may also provide therapeutic insights.