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

Tae In Kam, Youngdae Gwon, Yong Keun Jung

Research output: Contribution to journalReview articlepeer-review

Abstract

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.

Original languageEnglish (US)
Pages (from-to)4803-4813
Number of pages11
JournalCellular and Molecular Life Sciences
Volume71
Issue number24
DOIs
StatePublished - Aug 24 2014
Externally publishedYes

Keywords

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

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology
  • Pharmacology
  • Cellular and Molecular Neuroscience
  • Cell Biology

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