TY - JOUR
T1 - Accelerated accumulation of fibrinogen peptide chains with Aβ deposition in Alzheimer's disease (AD) mice and human AD brains
AU - Bian, Zhihong
AU - Yamashita, Toru
AU - Shi, Xiaowen
AU - Feng, Tian
AU - Yu, Haibo
AU - Hu, Xiao
AU - Hu, Xinran
AU - Bian, Yuting
AU - Sun, Hongming
AU - Tadokoro, Koh
AU - Takemoto, Mami
AU - Omote, Yosio
AU - Morihara, Ryuta
AU - Abe, Koji
N1 - Funding Information:
This study was partly supported by a Grant-in-Aid for Scientific Research (B) 17H0419611, (C) 20K09370, 17H0975609, and 17K1082709 and by Grants-in-Aid from the Research Committees (Kaji R, Toba K, and Tsuji S) from the Japan Agency for Medical Research and Development (7211700121, 7211800049 and 7211800130).
Publisher Copyright:
© 2021
PY - 2021/9/15
Y1 - 2021/9/15
N2 - Alzheimer's disease (AD) is a common neurodegenerative disease that is characterized by the abnormal accumulation of intracellular and extracellular amyloid-β (Aβ) as well as disruption of the blood brain barrier (BBB). Fibrinogen plays an essential role in regulating thrombosis, wound healing, and other biological functions. In the present study, we investigated the relationship between three polypeptide chains α, β, and γ (FGA, FGB, and FGG) and Aβ deposition in the APP23 plus chronic cerebral hypoperfusion (CCH) mice model as well as the human AD brain. FGA, FGB, and FGG accumulated when Aβ was deposited in neural cells and cerebral vessels. This deposition was significantly higher in AD plus CCH mice models relative to wild-type brains, and in human AD brains compared to control brains. The present study demonstrates that FGA, FGB, and FGG are associated with AD progress, and can thus be potential targets for the diagnosis and therapy of AD.
AB - Alzheimer's disease (AD) is a common neurodegenerative disease that is characterized by the abnormal accumulation of intracellular and extracellular amyloid-β (Aβ) as well as disruption of the blood brain barrier (BBB). Fibrinogen plays an essential role in regulating thrombosis, wound healing, and other biological functions. In the present study, we investigated the relationship between three polypeptide chains α, β, and γ (FGA, FGB, and FGG) and Aβ deposition in the APP23 plus chronic cerebral hypoperfusion (CCH) mice model as well as the human AD brain. FGA, FGB, and FGG accumulated when Aβ was deposited in neural cells and cerebral vessels. This deposition was significantly higher in AD plus CCH mice models relative to wild-type brains, and in human AD brains compared to control brains. The present study demonstrates that FGA, FGB, and FGG are associated with AD progress, and can thus be potential targets for the diagnosis and therapy of AD.
KW - Alzheimer's disease
KW - Cerebral amyloid angiopathy
KW - Chronic cerebral hypoperfusion
KW - Fibrinogen
KW - Human brain
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U2 - 10.1016/j.brainres.2021.147569
DO - 10.1016/j.brainres.2021.147569
M3 - Article
C2 - 34197775
AN - SCOPUS:85109459234
VL - 1767
JO - Molecular Brain Research
JF - Molecular Brain Research
SN - 0006-8993
M1 - 147569
ER -
