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Related Concept Videos

Alzheimer's Disease: Overview01:26

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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...
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Alzheimer Disease l: Introduction01:29

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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...
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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...
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Related Experiment Video

Updated: May 5, 2026

An In Vitro Model for the Study of Cellular Pathophysiology in Globoid Cell Leukodystrophy
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Alzheimer model chip with microglia BV2 cells.

Ehsan Yazdanpanah Moghadam1,2, Nahum Sonenberg2, Muthukumaran Packirisamy3

  • 1Optical-Bio Microsystems Laboratory, Micro-Nano-Bio Integration Center, Department of Mechanical and Industrial Engineering, Concordia University, Montreal, H3G 1M8, Canada.

Microsystems & Nanoengineering
|July 7, 2025
PubMed
Summary
This summary is machine-generated.

Amyloid beta oligomers (AβO) impact Alzheimer's Disease (AD) by altering microglia cell adhesion. This study used a microfluidic device to quantify AβO's effect on cell-substrate adhesion, revealing reduced adhesion with increased AβO concentration and incubation time.

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Area of Science:

  • Neuroscience
  • Biotechnology
  • Cell Biology

Background:

  • Amyloid beta oligomers (AβO) are key players in Alzheimer's Disease (AD) pathogenesis.
  • Microglia, the brain's immune cells, interact with AβO, influencing their mechanobiological properties.
  • Altered microglial adhesion strength is a potential biomarker for AD progression.

Purpose of the Study:

  • To develop and utilize a label-free microfluidic device as an in vitro model for detecting advancing AD conditions.
  • To quantitatively assess the impact of varying AβO concentrations on microglial cell-substrate adhesion strength.
  • To understand the mechanobiological changes in microglia upon exposure to AβO.

Main Methods:

  • A microfluidic device with a single channel was employed as a cell adhesion assay.
  • Microglia BV2 cells were exposed to different AβO concentrations (1 µM, 2.5 µM, 5 µM).
  • Cell-substrate adhesion was quantified in real-time under controlled flow shear stress (3 Pa and 7.5 Pa) using microscopy.

Main Results:

  • The microfluidic device successfully identified advancing AβO concentrations.
  • Increased incubation time with AβO led to reduced cell-substrate adhesion strength.
  • Higher AβO concentrations further weakened the adhesion of microglia to the substrate.

Conclusions:

  • Quantifying microglial cell-substrate adhesion in a microfluidic system serves as a viable method for modeling AD.
  • Mechanobiological changes in microglia, specifically adhesion strength, are sensitive indicators of AβO exposure and AD progression.
  • This approach offers a deeper understanding of microglia-AβO interactions in an in vitro AD model.