Feasibility of β-sheet breaker peptide-H102 treatment for Alzheimer's disease based on β-amyloid hypothesis.
β-amyloid hypothesis is the predominant hypothesis in the study of pathogenesis of Alzheimer's disease. This hypothesis claims that aggregation and neurotoxic effects of amyloid β (Aβ) is the common pathway in a variety of etiological factors for Alzheimer's disease. Aβ peptide derives from amyloid precursor protein (APP). β-sheet breaker peptides can directly prevent and reverse protein misfolding and aggregation in conformational disorders. Based on the stereochemical structure of Aβ1-42 and aggregation character, we had designed a series of β-sheet breaker peptides in our previous work and screened out a 10-residue peptide β-sheet breaker peptide, H102. We evaluated the effects of H102 on expression of P-tau, several associated proteins, inflammatory factors and apoptosis factors, and examined the cognitive ability of APP transgenic mice by behavioral test. This study aims to validate the β-amyloid hypothesis and provide an experimental evidence for the feasibility of H102 treatment for Alzheimer's disease.
2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, Key Laboratory of Hormone and Development (Ministry of Health), Metabolic Diseases Hospital and Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China.
Lai-xiang
LX
Lin
Department of physiology, Tianjin Medical University, Tianjin, China.
Xiang-yu
XY
Bo
Department of physiology, Tianjin Medical University, Tianjin, China.
Yuan-zhen
YZ
Tan
Department of physiology, Tianjin Medical University, Tianjin, China.
Feng-xian
FX
Sun
Department of physiology, Tianjin Medical University, Tianjin, China.
Ming
M
Song
Department of physiology, Tianjin Medical University, Tianjin, China.
Juan
J
Zhao
Department of physiology, Tianjin Medical University, Tianjin, China.
Zhi-hong
ZH
Ma
Department of physiology, Tianjin Medical University, Tianjin, China.
Mei
M
Li
Department of physiology, Tianjin Medical University, Tianjin, China.
Kai-jun
KJ
Zheng
Department of physiology, Tianjin Medical University, Tianjin, China.
Shu-Mei
SM
Xu
D000544:Alzheimer Disease / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D016564:Amyloid beta-Protein Precursor / Q000096:biosynthesis / Q000235:genetics; D000818:Animals; D006801:Humans; D051379:Mice; D008822:Mice, Transgenic; D008954:Models, Biological; D010455:Peptides / Q000737:chemistry / Q000235:genetics / Q000494:pharmacology*; D017433:Protein Structure, Secondary
C545487:APP protein, human; D016564:Amyloid beta-Protein Precursor; D010455:Peptides