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Related Experiment Video

Updated: Jan 26, 2026

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

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

Published on: July 14, 2010

Amyloid-β Oligomers Regulate ADAM10 Synaptic Localization Through Aberrant Plasticity Phenomena.

Elena Marcello¹, Stefano Musardo^2,3, Lina Vandermeulen²

¹Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Via Balzaretti 9, 20133, Milan, Italy. elena.marcello@unimi.it.

Molecular Neurobiology

|April 17, 2019

Summary

Alzheimer's disease (AD) oligomers disrupt synaptic plasticity by impairing ADAM10 internalization, a key enzyme in amyloid-β peptide regulation. This aberrant mechanism may downregulate amyloid-β generation while affecting structural plasticity.

Keywords:

ADAM10 Alzheimer disease Amyloid-β Synaptic plasticity

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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

Area of Science:

Neuroscience
Molecular Biology
Biochemistry

Background:

A disintegrin and metalloproteinase 10 (ADAM10) is a synaptic enzyme regulating amyloid-β (Aβ) peptide formation in Alzheimer's disease (AD).
ADAM10 activity is modulated by synaptic plasticity, with long-term depression (LTD) promoting its synaptic localization and long-term potentiation (LTP) causing its internalization.
ADAM10 plays a role in spine shaping via cleavage of adhesion molecules.

Purpose of the Study:

To investigate the effect of amyloid-β oligomers on ADAM10 synaptic localization and internalization.
To elucidate the mechanism by which Aβ oligomers influence ADAM10 trafficking at the synapse.
To understand the interplay between Aβ oligomers, synaptic plasticity, and ADAM10 function in AD pathogenesis.

Main Methods:

In vitro exposure of hippocampal neuronal cultures to Aβ oligomers.
Analysis of ADAM10 synaptic localization and endocytosis.
Investigation of the role of neuronal activity and NMDA receptor activation.

Main Results:

Aβ oligomers induced increased ADAM10 synaptic localization, similar to LTD, but through impaired endocytosis, not enhanced delivery.
Aβ oligomers inhibited ADAM10 internalization in a manner dependent on neuronal activity and NMDA receptor activation.
These findings suggest Aβ oligomers trigger an aberrant synaptic plasticity mechanism.

Conclusions:

Aβ oligomers can downregulate Aβ generation by modulating ADAM10 synaptic availability via impaired internalization.
Altered ADAM10 activity may impact structural plasticity, contributing to AD pathogenesis.
This study reveals a complex relationship between synaptic activity and core AD mechanisms involving ADAM10.