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Related Experiment Video

Updated: Jun 18, 2026

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

Preparation of Oligomeric β-amyloid_1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices

Published on: July 14, 2010

Alzheimer's disease: synaptic dysfunction and Abeta.

Ganesh M Shankar¹, Dominic M Walsh

¹Center for Neurologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA, USA. gshankar1@partners.org.

Molecular Neurodegeneration

|November 26, 2009

Summary

This summary is machine-generated.

Alzheimer's disease (AD) involves early synapse loss, leading to memory impairment. Soluble amyloid beta-protein (Abeta) forms are key culprits in this synaptic damage and potential therapeutic targets.

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Evaluation of Synapse Density in Hippocampal Rodent Brain Slices

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

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Evaluation of Synapse Density in Hippocampal Rodent Brain Slices

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices

Published on: October 6, 2017

Area of Science:

Neuroscience
Neuropathology
Molecular Biology

Background:

Synapse loss is an early hallmark of Alzheimer's disease (AD), correlating with dementia severity.
Disrupted neural plasticity contributes to memory deficits and eventual cell loss in AD.

Purpose of the Study:

To review evidence implicating soluble amyloid beta-protein (Abeta) in synaptic compromise in AD.
To discuss mechanisms of Abeta-induced synaptotoxicity.
To identify potential therapeutic targets for AD.

Main Methods:

Review of multi-disciplinary research on Alzheimer's disease.
Analysis of studies on amyloid beta-protein (Abeta) and its role in synaptic function.
Examination of mechanisms underlying Abeta synaptotoxicity.

Main Results:

Non-fibrillar soluble forms of Abeta are identified as mediators of synaptic compromise in AD.
Evidence suggests Abeta directly impacts synaptic integrity and function.
Potential pathways for Abeta-induced neuronal damage are highlighted.

Conclusions:

Soluble Abeta species are critical in mediating synapse loss and dysfunction in Alzheimer's disease.
Understanding Abeta synaptotoxicity mechanisms is crucial for developing effective AD therapies.
Targeting Abeta-mediated synaptic damage offers a promising therapeutic strategy for AD.