Related Experiment Video

Updated: Jun 18, 2026

Neurodegeneration in an Animal Model of Chronic Amyloid-beta Oligomer Infusion Is Counteracted by Antibody Treatment Infused with Osmotic Pumps
10:19

Neurodegeneration in an Animal Model of Chronic Amyloid-beta Oligomer Infusion Is Counteracted by Antibody Treatment Infused with Osmotic Pumps

Published on: August 14, 2016

Beta-amyloid oligomers and cellular prion protein in Alzheimer's disease

Erik C Gunther1, Stephen M Strittmatter

  • 1Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, 295 Congress Ave., BCMM 436, New Haven, CT 06536-0812, USA.

Journal of Molecular Medicine (Berlin, Germany)
|December 5, 2009
PubMed

Insights

Prefibrillar beta-amyloid (A beta) oligomers are key in Alzheimer's disease (AD) progression. The cellular prion protein (PrP(C)) acts as a receptor for these A beta oligomers, revealing links between AD and prion diseases.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Pathology

Background:

  • Prefibrillar oligomers of beta-amyloid (A beta) are implicated in Alzheimer's disease (AD) pathophysiology.
  • Oligomeric A beta assemblies, not monomers or plaques, are linked to synaptic deficits, neurotoxicity, and AD progression.
  • The molecular targets of A beta oligomer action remain largely unidentified.

Purpose of the Study:

  • To review the significance of A beta oligomers in AD.
  • To explore commonalities between Alzheimer's disease and Creutzfeldt-Jakob Disease (CJD).
  • To highlight the emerging role of cellular prion protein (PrP(C)) as a receptor for A beta oligomers.

Main Methods:

  • Literature review of studies on A beta oligomers, AD, CJD, and PrP(C).

Main Results:

  • A beta oligomers are critical mediators of AD.
  • Cellular prion protein (PrP(C)) functions as a receptor for A beta oligomers in brain slices.
  • Mechanistic similarities exist between AD and CJD.

Conclusions:

  • A beta oligomers are central to AD pathogenesis.
  • PrP(C) acts as a functional receptor for neurotoxic A beta oligomers.
  • The interaction between A beta oligomers and PrP(C) suggests shared pathways in neurodegeneration.

More Related Videos

A11-positive β-amyloid Oligomer Preparation and Assessment Using Dot Blotting Analysis06:17

A11-positive β-amyloid Oligomer Preparation and Assessment Using Dot Blotting Analysis

Published on: May 22, 2018

Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus08:16

Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus

Published on: June 17, 2015

Related Concept Videos

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