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Related Experiment Video

Updated: Feb 3, 2026

Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry

Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry

Published on: March 7, 2019

Endogenous amyloid-β mediates memory forgetting in the normal brain.

Sukwon Lee¹, Jeongyeon Kim¹, Sukwoo Choi²

¹School of Biological Sciences, Seoul National University, Seoul, South Korea; Department of Neural Development and Disease, Korea Brain Research Institute, Daegu, South Korea.

Biochemical and Biophysical Research Communications

|October 27, 2018

Summary

Amyloid beta (Aβ) is essential for memory forgetting in healthy brains. Blocking Aβ with antibodies or in specific mouse models prolonged memory retention, revealing its role in normal cognitive function.

Keywords:

Amyloid beta Forgetting IgG Fcγ receptor II-b Long-term memory Object recognition memory

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Assaying β-amyloid Toxicity using a Transgenic C. elegans Model

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Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry

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Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits

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Assaying β-amyloid Toxicity using a Transgenic C. elegans Model

Assaying β-amyloid Toxicity using a Transgenic C. elegans Model

Published on: October 9, 2010

Area of Science:

Neuroscience
Molecular Biology
Cognitive Science

Background:

Amyloid beta (Aβ) is a key molecule implicated in Alzheimer's disease pathophysiology.
The precise function of Aβ in the normal brain remains largely unknown.

Purpose of the Study:

To investigate the role of endogenous Amyloid beta (Aβ) in memory processes within the healthy brain.
To determine if Aβ is involved in memory forgetting or consolidation.

Main Methods:

Monitoring object recognition memory in mice.
Microinjection of anti-Aβ antibody (4G8) into brain ventricles to neutralize soluble Aβ.
Utilizing Fcgr2b knockout (KO) mice lacking a receptor for soluble Aβ oligomers.

Main Results:

Microinjection of anti-Aβ antibody after memory acquisition significantly prolonged memory maintenance.
The antibody's effect on memory maintenance persisted even when injected after the memory consolidation phase.
Fcgr2b KO mice exhibited prolonged object recognition memory maintenance, suggesting a role for Aβ-FcγRIIb interactions.

Conclusions:

Endogenous Amyloid beta (Aβ) plays a crucial role in the natural process of memory forgetting in the normal brain.
Aβ actively contributes to the decay of memory traces, rather than solely being involved in pathology.
These findings offer new insights into the physiological functions of Aβ in cognition.