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Updated: May 21, 2026

Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus
Published on: June 17, 2015
Viewpoint: Crosstalks between neurofibrillary tangles and amyloid plaque formation
Kailie Luan1, Jesusa L Rosales, Ki-Young Lee
1Department of Cell Biology and Anatomy, Southern Alberta Cancer Research and Hotchkiss Brain Institutes, University of Calgary, Alberta, Canada.
Alzheimer's disease (AD) involves amyloid plaques and neurofibrillary tangles (NFTs). This review explores five mechanisms detailing how these pathologies interact, offering new therapeutic targets for AD.
Area of Science:
- Neuroscience
- Pathology
- Biochemistry
Background:
- Alzheimer's disease (AD) is characterized by amyloid plaques and neurofibrillary tangles (NFTs).
- Evidence suggests an interplay between beta-amyloid (Aβ) and tau pathologies in AD.
- The precise mechanisms linking these hallmarks remain unclear.
Purpose of the Study:
- To review recent evidence on the crosstalk between amyloid plaque and NFT formation in AD pathogenesis.
- To elucidate five putative mechanisms driving the interaction of these pathologies.
- To identify potential therapeutic strategies based on understanding these crosstalks.
Main Methods:
- Literature review of recent studies on AD pathogenesis.
- Analysis of evidence supporting mechanisms of interaction between Aβ and tau.
- Synthesis of findings to propose five crosstalk mechanisms.
Main Results:
- Five putative mechanisms of crosstalk between amyloid plaques and NFTs are discussed.
- Aβ internalization and intracellular generation can accelerate NFT formation.
- Tau elements influence Aβ and amyloid plaque formation.
Conclusions:
- Understanding the crosstalk between amyloid plaques and NFTs is crucial for AD pathogenesis.
- Elucidating these mechanisms may reveal novel therapeutic targets.
- Targeting the interplay between these pathologies could offer new strategies to delay or halt AD progression.
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