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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...
The Blood-brain Barrier00:49

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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...
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...
Dementia l: Introduction01:22

Dementia l: Introduction

Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...

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Updated: Jun 23, 2026

In Vitro Assays to Assess Blood-brain Barrier Mesh-like Vessel Formation and Disruption
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In Vitro Assays to Assess Blood-brain Barrier Mesh-like Vessel Formation and Disruption

Published on: June 20, 2017

Beta-amyloid, blood vessels, and brain function.

Eric E Smith1, Steven M Greenberg

  • 1Division of Neurology, Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta, Canada.

Stroke
|May 16, 2009
PubMed
Summary
This summary is machine-generated.

Alzheimer disease and cerebrovascular disease often coexist. Beta-amyloid, central to Alzheimer

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Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry
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Analysis of β-Amyloid-induced Abnormalities on Fibrin Clot Structure by Spectroscopy and Scanning Electron Microscopy
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Analysis of β-Amyloid-induced Abnormalities on Fibrin Clot Structure by Spectroscopy and Scanning Electron Microscopy

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Related Experiment Videos

Last Updated: Jun 23, 2026

In Vitro Assays to Assess Blood-brain Barrier Mesh-like Vessel Formation and Disruption
10:36

In Vitro Assays to Assess Blood-brain Barrier Mesh-like Vessel Formation and Disruption

Published on: June 20, 2017

Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry
09:31

Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry

Published on: March 7, 2019

Analysis of β-Amyloid-induced Abnormalities on Fibrin Clot Structure by Spectroscopy and Scanning Electron Microscopy
06:27

Analysis of β-Amyloid-induced Abnormalities on Fibrin Clot Structure by Spectroscopy and Scanning Electron Microscopy

Published on: November 30, 2018

Area of Science:

  • Neurology
  • Gerontology
  • Pathology

Background:

  • Alzheimer disease (AD) and cerebrovascular disease (CVD) are common aging-related conditions frequently found together.
  • Brain infarction, including silent infarction, impacts AD progression.
  • Beta-amyloid (Aβ) may impair cerebrovascular function, and cerebral amyloid angiopathy (CAA) is linked to vascular dysfunction.

Purpose of the Study:

  • To review the current evidence linking beta-amyloid metabolism with vascular function and morphological changes.
  • To explore the interplay between Alzheimer disease pathology and cerebrovascular integrity.

Main Methods:

  • Literature review of animal and human studies.
  • Analysis of research on beta-amyloid deposition and vascular effects.
  • Examination of morphological changes in cerebral capillaries associated with AD.

Main Results:

  • Evidence suggests beta-amyloid accumulation affects vascular health.
  • Soluble beta-amyloid can disrupt normal vascular responses.
  • Cerebral amyloid angiopathy is associated with impaired blood vessel function in both animal models and humans.

Conclusions:

  • Beta-amyloid metabolism is intricately linked to cerebrovascular function and structure.
  • Understanding this relationship is crucial for managing coexisting Alzheimer disease and cerebrovascular disease.
  • Further research is needed to elucidate the mechanisms driving these interactions.