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

作者：Kam Tae In; Gwon Youngdae; Jung Yong Keun^*

来源：Cellular and Molecular Life Sciences, 2014, 71(24): 4803-4813.

DOI：10.1007/s00018-014-1706-0

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

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

• 出版日期2014-12