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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...
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...
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...

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Related Experiment Video

Updated: May 19, 2026

Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons
06:23

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Published on: October 30, 2018

Interaction between amyloid-β pathology and cortical functional columnar organization.

Shlomit Beker1, Vered Kellner, Lucia Kerti

  • 1Brain Research Center, Faculty of Life Sciences, Bar-Ilan University, Ramat Gan, 52900 Israel.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|August 17, 2012
PubMed
Summary

Alzheimer's disease (AD) research shows amyloid-β plaques disrupt brain connectivity. Plaques concentrate in specific cortical areas, not randomly, impacting neural networks and potentially explaining AD symptoms.

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Establishment of a Valuable Mimic of Alzheimer's Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein
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Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus
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Related Experiment Videos

Last Updated: May 19, 2026

Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons
06:23

Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons

Published on: October 30, 2018

Establishment of a Valuable Mimic of Alzheimer's Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein
08:27

Establishment of a Valuable Mimic of Alzheimer's Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein

Published on: July 29, 2018

Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus
08:16

Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus

Published on: June 17, 2015

Area of Science:

  • Neuroscience
  • Neuropathology
  • Alzheimer's Disease Research

Background:

  • Amyloid-β plaques are a key hallmark of Alzheimer's disease (AD).
  • These plaques disrupt neuronal connectivity, potentially causing AD symptoms.
  • Understanding plaque distribution relative to neural networks is crucial for AD research.

Purpose of the Study:

  • To investigate the distribution and clustering patterns of amyloid-β plaques in the primary sensory cortex (barrel cortex).
  • To correlate plaque distribution with the anatomical structure of the barrel cortex and functional columns.
  • To compare plaque clustering in somatosensory versus visual cortex in AD.

Main Methods:

  • Quantitative analysis of amyloid-β plaque distribution and clustering within the barrel cortex (Layer IV) and its supragranular extensions.
  • Comparison of plaque distribution patterns between barrels and septal areas.
  • Comparative analysis of plaque clustering in somatosensory cortex versus visual cortex.

Main Results:

  • Amyloid-β plaques were not randomly distributed in the barrel cortex; they concentrated in septal areas over barrels in Layer IV.
  • This septal concentration was not observed in supragranular extensions of functional columns.
  • Plaque clustering was significantly higher in the somatosensory cortex compared to the visual cortex, a difference maintained in Layers II/III.

Conclusions:

  • The anatomical discontinuity of cortical areas correlates with neuropathological deposit patterns in Alzheimer's disease.
  • Plaque distribution is non-random and linked to specific cortical structures.
  • These findings suggest predictable patterns of computational disruption in the AD brain based on plaque localization.