Related Experiment Video

Updated: Jun 11, 2026

Preparation of Oligomeric β-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

Amyloid β1-42 oligomer inhibits myelin sheet formation in vitro

Makoto Horiuchi1, Izumi Maezawa, Aki Itoh

  • 1Department of Neurology, University of California Davis, School of Medicine, Sacramento, CA 95817, United States.

Neurobiology of Aging
|July 3, 2010
PubMed

Insights

Alzheimer's disease amyloid-beta oligomers damage mature oligodendrocytes, impairing myelin maintenance and repair. This white matter damage contributes to neural disconnections in Alzheimer's disease.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Alzheimer's Disease Research

Background:

  • White matter degeneration is a key feature of Alzheimer's disease (AD), leading to neural disconnections.
  • While neuronal loss contributes, the role of amyloid-beta (Aβ) in damaging oligodendrocytes, the myelin-producing cells, is under investigation.

Purpose of the Study:

  • To investigate the effects of soluble oligomeric amyloid-beta (Aβ) on oligodendrocyte survival and differentiation.
  • To determine if Aβ oligomers contribute to white matter damage in AD pathophysiology.

Main Methods:

  • Utilized highly purified rat oligodendroglial lineage cell cultures at various developmental stages.
  • Assessed oligodendrocyte survival and differentiation following exposure to specific concentrations of Aβ oligomers.
  • Measured cell viability using MTT assay and evaluated myelin sheet formation in vitro.

Main Results:

  • Oligomeric Aβ (≥10 μM) significantly reduced mature oligodendrocyte survival.
  • Oligodendroglial progenitor cells (OPCs) showed relative resistance to Aβ oligomer cytotoxicity.
  • Aβ oligomers (≥1 μM) accelerated MTT formazan exocytosis in mature oligodendrocytes and inhibited myelin formation during OPC differentiation.

Conclusions:

  • Oligomeric Aβ directly damages mature oligodendrocytes and impairs myelin formation and maintenance.
  • This Aβ-mediated oligodendrocyte damage represents a novel mechanism contributing to white matter degeneration in AD.
  • The findings suggest impaired myelin maintenance and remyelination by OPCs, leading to axonal damage and neural disconnections.

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

Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons06:23

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

Published on: October 30, 2018

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...
Nervous Tissue: Myelin01:25

Nervous Tissue: Myelin

The myelin sheath is a multilayered lipid and protein covering that insulates the axon of a neuron, enhancing the speed of nerve impulse conduction. Axons without this sheath are referred to as unmyelinated. Two types of neuroglia, Schwann cells in the peripheral nervous system (PNS) and oligodendrocytes in the central nervous system (CNS) are responsible for producing myelin sheaths.
Schwann cells begin to form myelin sheaths around axons during fetal development. They wrap around a small...