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Related Experiment Video

Updated: Nov 25, 2025

Preparation of Oligomeric &#946;-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices
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REDD1 Is Involved in Amyloid β-Induced Synaptic Dysfunction and Memory Impairment.

Jee Hyun Yi1, Huiyoung Kwon2, Eunbi Cho2

  • 1Center for Synaptic Brain Dysfunctions, Institute for Basic Science, Daejeon 34141, Korea.

International Journal of Molecular Sciences
|December 16, 2020
PubMed
Summary

Protein REDD1 (regulated in development and DNA damage response 1) is upregulated by amyloid beta (Aβ) and contributes to Alzheimer's disease (AD) pathology, including memory deficits. Targeting REDD1 may offer a new therapeutic strategy for AD.

Keywords:
Alzheimer’s diseaseAβREDD1hippocampal long-term potentiationlearning and memory

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Alzheimer's disease (AD) is characterized by amyloid beta (Aβ) accumulation and neurodegeneration.
  • The role of protein REDD1 (regulated in development and DNA damage response 1) in Aβ pathology and AD pathogenesis remains unclear.
  • Understanding REDD1's involvement is crucial for developing novel AD therapeutics.

Purpose of the Study:

  • To investigate how Aβ influences REDD1 levels in the brain.
  • To determine if REDD1 mediates Aβ-induced synaptic dysfunction.
  • To evaluate the therapeutic potential of targeting REDD1 in an AD mouse model.

Main Methods:

  • Examined REDD1 expression in mouse hippocampal slices and brains following Aβ exposure.
  • Utilized short hairpin RNA (shRNA) to inhibit REDD1 expression.
  • Assessed synaptic plasticity and memory function in AD-like mouse models with REDD1 inhibition.

Main Results:

  • Aβ exposure increased REDD1 levels in hippocampal slices and brains, suggesting translational regulation.
  • Aβ-induced REDD1 upregulation involved the Fyn/ERK/S6 and mGluR5 pathways.
  • REDD1 inhibition via shRNA ameliorated Aβ-induced synaptic deficits and memory impairment in mice.

Conclusions:

  • REDD1 plays a significant role in Aβ-induced synaptic dysfunction and memory deficits.
  • REDD1 is a potential therapeutic target for Alzheimer's disease.
  • Further research into REDD1 modulation could lead to effective AD treatments.