Alzheimer’s disease: amyloid-based pathogenesis and potential therapies
Authors:Yixiu Zhou1, Yuhui Sun2, Quan-Hong Ma2 and Yaobo Liu2
1 Medical College of Soochow University, Soochow University, Suzhou, Jiangsu 215004, China.
2 Jiangsu Key Laboratory of Neuropsychiatric Diseases and Institute of Neuroscience, Soochow University, Suzhou, Jiangsu 215123, China.
Keywords:
Alzheimer’s disease (AD), amyloid β (Aβ), synapses, neural circuits, treatment.
Abbreviations:
Aβ – amyloid β,
AD – Alzheimer’s disease,
APP – amyloid precursor protein,
BBB – blood-brain barrier,
FAD – familial AD,
LDLR – low-density lipoprotein receptor,
LTD – long-term depression,
LTP – long-term potentiation,
NMDA – N-methyl-D-aspartic acid
NMDAR – NMDA receptor, PrPc – cellular prion protein.
Corresponding Author(s):
Conflict of interest statement:
The authors declare no competing financial interests.
Please cite this article as:
Yixiu Zhou, Yuhui Sun, Quan-Hong Ma and Yaobo Liu (2018). Alzheimer’s disease: amyloid-based pathogenesis and potential therapies. Cell Stress 2(7): 150-161. doi: 10.15698/cst2018.07.143
Yixiu Zhou, Yuhui Sun, Quan-Hong Ma and Yaobo Liu (2018). Alzheimer’s disease: amyloid-based pathogenesis and potential therapies. Cell Stress: in press.
Abstract:
Alzheimer’s disease is one of the most severe neurodegenerative diseases among elderly people. Different pathogenic factors for Alzheimer’s disease have been posited and studied in recent decades, but no effective treatment has been found, necessitating further studies. In this Viewpoint article, we assess studies on the mechanisms underlying the accumulation of amyloid b (Aβ) peptide and the formation of Aβ oligomers because their accumulation in amyloid plaques in brain tissue has become a well-studied hallmark of Alzheimer’s disease. We focus on the production of Aβ and its impact on the function of synapses and neural circuits, and also discuss the clinical prospects for amyloid-targeted therapies.