Cellular and Molecular Life Sciences

, Volume 71, Issue 24, pp 4803–4813

Amyloid beta receptors responsible for neurotoxicity and cellular defects in Alzheimer’s disease


DOI: 10.1007/s00018-014-1706-0

Cite this article as:
Kam, TI., Gwon, Y. & Jung, YK. Cell. Mol. Life Sci. (2014) 71: 4803. doi:10.1007/s00018-014-1706-0


Alzheimer’s disease (AD) is the most common neurodegenerative disease. Although a major cause of AD is the accumulation of amyloid-β (Aβ) peptide that induces neuronal loss and cognitive impairments, our understanding of its neurotoxic mechanisms is limited. Recent studies have identified putative Aβ-binding receptors that mediate Aβ neurotoxicity in cells and models of AD. Once Aβ interacts with a receptor, a toxic signal is transduced into neurons, resulting in cellular defects including endoplasmic reticulum stress and mitochondrial dysfunction. In addition, Aβ can also be internalized into neurons through unidentified Aβ receptors and induces malfunction of subcellular organelles, which explains some part of Aβ neurotoxicity. Understanding the neurotoxic signaling initiated by Aβ-receptor binding and cellular defects provide insight into new therapeutic windows for AD. In the present review, we summarize the findings on Aβ-binding receptors and the neurotoxicity of oligomeric Aβ.


Amyloid beta Alzheimer’s disease Aβ receptor Neurotoxicity Uptake Mitochondria ER stress 

Copyright information

© Springer Basel 2014

Authors and Affiliations

  1. 1.Global Research Laboratory, School of Biological SciencesSeoul National UniversitySeoulKorea

Personalised recommendations