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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...
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...
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 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...
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...

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Related Experiment Video

Updated: May 29, 2026

Preparation of Oligomeric &beta;-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices
04:41

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices

Published on: July 14, 2010

[Alzheimer's disease, amyloid peptide and synaptic dysfunction].

Agnès Hémar1, Christophe Mulle

  • 1Institut interdisciplinaire de neurosciences, Université de Bordeaux, Bordeaux Cedex, France. ahemar@u-bordeaux2.fr

Medecine Sciences : M/S
|September 2, 2011
PubMed
Summary

Alzheimer's disease (AD) involves memory loss due to amyloid-beta (Aβ) oligomers disrupting brain cell connections. Research explores how Aβ oligomers impair synaptic function, leading to cognitive decline in early AD.

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Last Updated: May 29, 2026

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Area of Science:

  • Neuroscience
  • Pathology

Context:

  • Alzheimer's disease (AD) is a leading cause of dementia.
  • Early AD stages correlate memory impairment with amyloid-beta (Aβ) oligomers in the cortex.

Purpose:

  • To review research on synaptic dysfunction mechanisms in early AD.
  • To understand the consequences of Aβ oligomers on neural circuit activity.

Summary:

  • Soluble amyloid-beta (Aβ) oligomers are implicated in early Alzheimer's disease (AD) and memory loss.
  • Aβ oligomers disrupt glutamatergic synaptic function, impairing neural plasticity and cognitive abilities.
  • Rodent studies confirm Aβ oligomers impair synaptic transmission and cause cognitive deficits.

Impact:

  • Understanding Aβ oligomer pathways is crucial for developing early AD interventions.
  • This review highlights the need for further research into synaptic dysfunction mechanisms in AD.