Blood-derived amyloid-β protein induces Alzheimer's disease pathologies
The amyloid-β protein (Aβ) protein plays a pivotal role in the pathogenesis of Alzheimer's disease (AD). It is believed that Aβ deposited in the brain originates from the brain tissue itself. However, Aβ is generated in both brain and peripheral tissues. Whether circulating Aβ contributes to br...
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| Published in: | Molecular psychiatry Vol. 23; no. 9; pp. 1948 - 1956 |
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| Main Authors: | , , , , , , , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
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Nature Publishing Group
01.09.2018
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| ISSN: | 1359-4184, 1476-5578, 1476-5578 |
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| Abstract | The amyloid-β protein (Aβ) protein plays a pivotal role in the pathogenesis of Alzheimer's disease (AD). It is believed that Aβ deposited in the brain originates from the brain tissue itself. However, Aβ is generated in both brain and peripheral tissues. Whether circulating Aβ contributes to brain AD-type pathologies remains largely unknown. In this study, using a model of parabiosis between APPswe/PS1dE9 transgenic AD mice and their wild-type littermates, we observed that the human Aβ originated from transgenic AD model mice entered the circulation and accumulated in the brains of wild-type mice, and formed cerebral amyloid angiopathy and Aβ plaques after a 12-month period of parabiosis. AD-type pathologies related to the Aβ accumulation including tau hyperphosphorylation, neurodegeneration, neuroinflammation and microhemorrhage were found in the brains of the parabiotic wild-type mice. More importantly, hippocampal CA1 long-term potentiation was markedly impaired in parabiotic wild-type mice. To the best of our knowledge, our study is the first to reveal that blood-derived Aβ can enter the brain, form the Aβ-related pathologies and induce functional deficits of neurons. Our study provides novel insight into AD pathogenesis and provides evidence that supports the development of therapies for AD by targeting Aβ metabolism in both the brain and the periphery. |
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| AbstractList | The amyloid-β protein (Aβ) protein plays a pivotal role in the pathogenesis of Alzheimer's disease (AD). It is believed that Aβ deposited in the brain originates from the brain tissue itself. However, Aβ is generated in both brain and peripheral tissues. Whether circulating Aβ contributes to brain AD-type pathologies remains largely unknown. In this study, using a model of parabiosis between APPswe/PS1dE9 transgenic AD mice and their wild-type littermates, we observed that the human Aβ originated from transgenic AD model mice entered the circulation and accumulated in the brains of wild-type mice, and formed cerebral amyloid angiopathy and Aβ plaques after a 12-month period of parabiosis. AD-type pathologies related to the Aβ accumulation including tau hyperphosphorylation, neurodegeneration, neuroinflammation and microhemorrhage were found in the brains of the parabiotic wild-type mice. More importantly, hippocampal CA1 long-term potentiation was markedly impaired in parabiotic wild-type mice. To the best of our knowledge, our study is the first to reveal that blood-derived Aβ can enter the brain, form the Aβ-related pathologies and induce functional deficits of neurons. Our study provides novel insight into AD pathogenesis and provides evidence that supports the development of therapies for AD by targeting Aβ metabolism in both the brain and the periphery. The amyloid-β protein (Aβ) protein plays a pivotal role in the pathogenesis of Alzheimer's disease (AD). It is believed that Aβ deposited in the brain originates from the brain tissue itself. However, Aβ is generated in both brain and peripheral tissues. Whether circulating Aβ contributes to brain AD-type pathologies remains largely unknown. In this study, using a model of parabiosis between APPswe/PS1dE9 transgenic AD mice and their wild-type littermates, we observed that the human Aβ originated from transgenic AD model mice entered the circulation and accumulated in the brains of wild-type mice, and formed cerebral amyloid angiopathy and Aβ plaques after a 12-month period of parabiosis. AD-type pathologies related to the Aβ accumulation including tau hyperphosphorylation, neurodegeneration, neuroinflammation and microhemorrhage were found in the brains of the parabiotic wild-type mice. More importantly, hippocampal CA1 long-term potentiation was markedly impaired in parabiotic wild-type mice. To the best of our knowledge, our study is the first to reveal that blood-derived Aβ can enter the brain, form the Aβ-related pathologies and induce functional deficits of neurons. Our study provides novel insight into AD pathogenesis and provides evidence that supports the development of therapies for AD by targeting Aβ metabolism in both the brain and the periphery.The amyloid-β protein (Aβ) protein plays a pivotal role in the pathogenesis of Alzheimer's disease (AD). It is believed that Aβ deposited in the brain originates from the brain tissue itself. However, Aβ is generated in both brain and peripheral tissues. Whether circulating Aβ contributes to brain AD-type pathologies remains largely unknown. In this study, using a model of parabiosis between APPswe/PS1dE9 transgenic AD mice and their wild-type littermates, we observed that the human Aβ originated from transgenic AD model mice entered the circulation and accumulated in the brains of wild-type mice, and formed cerebral amyloid angiopathy and Aβ plaques after a 12-month period of parabiosis. AD-type pathologies related to the Aβ accumulation including tau hyperphosphorylation, neurodegeneration, neuroinflammation and microhemorrhage were found in the brains of the parabiotic wild-type mice. More importantly, hippocampal CA1 long-term potentiation was markedly impaired in parabiotic wild-type mice. To the best of our knowledge, our study is the first to reveal that blood-derived Aβ can enter the brain, form the Aβ-related pathologies and induce functional deficits of neurons. Our study provides novel insight into AD pathogenesis and provides evidence that supports the development of therapies for AD by targeting Aβ metabolism in both the brain and the periphery. |
| Author | Liu, Y-H Song, W Xiang, Y Chen, S-H Dong, Z-F Zhou, H-D Shen, L-L Zeng, F Chen, X-W Yao, X-Q Jin, W-S Sun, H-L Bu, X-L Shan, Y-C Wang, J Liu, J-H Huang, Z-L Zhuang, Z-Q Giunta, B Tan, J Zhou, X-F Zhang, K Wang, Y-J |
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Military Medical University, Chongqing, China – sequence: 6 givenname: Z-L surname: Huang fullname: Huang, Z-L organization: Ministry of Education Key Laboratory of Child Development and Disorders and Chongqing Key Laboratory of Translational Medical Research in Cognitive Development and Learning and Memory Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China – sequence: 7 givenname: K surname: Zhang fullname: Zhang, K organization: Brain Research Center and State Key Laboratory of Trauma, Burns and Combined Injury, Third Military Medical University, Chongqing, China – sequence: 8 givenname: Y-H surname: Liu fullname: Liu, Y-H organization: Department of Neurology and Centre for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, China – sequence: 9 givenname: F surname: Zeng fullname: Zeng, F organization: Department of Neurology and Centre for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, China – sequence: 10 givenname: J-H surname: Liu fullname: Liu, J-H organization: University of Chinese Academy of Sciences, Beijing, China – sequence: 11 givenname: H-L surname: Sun fullname: Sun, H-L organization: Department of Neurology and Centre for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, China – sequence: 12 givenname: Z-Q surname: Zhuang fullname: Zhuang, Z-Q organization: Department of Neurology and Centre for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, China – sequence: 13 givenname: S-H surname: Chen fullname: Chen, S-H organization: Department of Neurology and Centre for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, China – sequence: 14 givenname: X-Q surname: Yao fullname: Yao, X-Q organization: Department of Neurology and Centre for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, China – sequence: 15 givenname: B surname: Giunta fullname: Giunta, B organization: Neuroimmunology Laboratory, Department of Psychiatry and Behavioral Neurosciences, Morsani College of Medicine, University of South Florida, Tampa, FL, USA – sequence: 16 givenname: Y-C surname: Shan fullname: Shan, Y-C organization: CAS Key Laboratory of Separation Sciences for Analytical Chemistry, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian, China – sequence: 17 givenname: J surname: Tan fullname: Tan, J organization: Rashid Laboratory for Developmental Neurobiology, Silver Child Development Center, Department of Psychiatry and Behavioral Neurosciences, Morsani College of Medicine, University of South Florida, Tampa, FL, USA – sequence: 18 givenname: X-W surname: Chen fullname: Chen, X-W organization: Brain Research Center and State Key Laboratory of Trauma, Burns and Combined Injury, Third Military Medical University, Chongqing, China – sequence: 19 givenname: Z-F surname: Dong fullname: Dong, Z-F organization: Ministry of Education Key Laboratory of Child Development and Disorders and Chongqing Key Laboratory of Translational Medical Research in Cognitive Development and Learning and Memory Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China – sequence: 20 givenname: H-D surname: Zhou fullname: Zhou, H-D organization: Department of Neurology and Centre for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, China – sequence: 21 givenname: X-F surname: Zhou fullname: Zhou, X-F organization: School of Pharmacy and Medical Sciences and Sansom Institute, University of South Australia, Adelaide, SA, Australia – sequence: 22 givenname: W surname: Song fullname: Song, W email: weihong@mail.ubc.ca organization: Townsend Family Laboratories, Department of Psychiatry, The University of British Columbia, Vancouver, BC, Canada. weihong@mail.ubc.ca – sequence: 23 givenname: Y-J surname: Wang fullname: Wang, Y-J email: yanjiang_wang@tmmu.edu.cn organization: Department of Neurology and Centre for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, China. yanjiang_wang@tmmu.edu.cn |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29086767$$D View this record in MEDLINE/PubMed |
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| Snippet | The amyloid-β protein (Aβ) protein plays a pivotal role in the pathogenesis of Alzheimer's disease (AD). It is believed that Aβ deposited in the brain... The amyloid-β protein (Aβ) protein plays a pivotal role in the pathogenesis of Alzheimer’s disease (AD). It is believed that Aβ deposited in the brain... |
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| SubjectTerms | Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer's disease Amyloid beta-Peptides - blood Amyloid beta-Peptides - metabolism Amyloid beta-Peptides - physiology Amyloid beta-Protein Precursor - metabolism Animals Blood Brain Brain - metabolism Brain - pathology Cerebral amyloid angiopathy Cerebral Amyloid Angiopathy - metabolism Cerebral blood flow Disease Models, Animal Female Hippocampus Hippocampus - metabolism Inflammation Long-term potentiation Male Mice Mice, Inbred C57BL Mice, Transgenic Neurodegeneration Neurons - metabolism Parabiosis Parabiosis - methods Pathogenesis Phosphorylation Plaque, Amyloid - etiology Plaque, Amyloid - metabolism Presenilin-1 - metabolism Proteins Rodents Senile plaques Tau protein Transgenic mice |
| Title | Blood-derived amyloid-β protein induces Alzheimer's disease pathologies |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/29086767 https://www.proquest.com/docview/2132257584 https://www.proquest.com/docview/1958536653 |
| Volume | 23 |
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