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231225s2021 xx |||||o 00| ||eng c |
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7 |
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|a 10.1002/adma.202006483
|2 doi
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|a pubmed24n1514.xml
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|a (NLM)33325586
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|a DE-627
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|c DE-627
|e rakwb
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| 041 |
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|a eng
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| 100 |
1 |
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|a Wang, Hui
|e verfasserin
|4 aut
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| 245 |
1 |
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|a Recognition and Removal of Amyloid-β by a Heteromultivalent Macrocyclic Coassembly
|b A Potential Strategy for the Treatment of Alzheimer's Disease
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| 264 |
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|c 2021
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| 336 |
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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| 338 |
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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| 500 |
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|a Date Completed 24.07.2024
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|a Date Revised 27.08.2024
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a © 2020 Wiley-VCH GmbH.
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|a The imbalance of amyloid-β (Aβ) production and clearance causes aggregation of Aβ1-42 monomers to form fibrils and amyloid plaques, which is an indispensable process in the pathogenesis of Alzheimer's disease (AD), and eventually leads to pathological changes and cognitive impairment. Consequently, Aβ1-42 is the most important target for the treatment of AD. However, developing a single treatment method that can recognize Aβ1-42 , inhibit Aβ1-42 fibrillation, eliminate amyloid plaques, improve cognitive impairments, and alleviate AD-like pathology is challenging. Here, a coassembly composed of cyclodextrin (CD) and calixarene (CA) is designed, and it is used as an anti-Aβ therapy agent. The CD-CA coassembly is based on the previously reported heteromultivalent recognition strategy and is able to successfully eliminate amyloid plaques and degrade Aβ1-42 monomers in 5xFAD mice. More importantly, the coassembly improves recognition and spatial cognition deficits, and synaptic plasticity impairment in the 5xFAD mice. In addition, the coassembly ameliorates AD-like pathology including prevention of neuronal apoptosis and oxidant stress, and alteration of M1/M2 microglial polarization states. This supramolecular approach makes full use of both molecular recognition and self-assembly of macrocyclic amphiphiles, and is a promising novel strategy for AD treatment
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|a Journal Article
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|a Alzheimer's disease
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| 650 |
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|a amyloid plaques
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| 650 |
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4 |
|a cognition
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| 650 |
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4 |
|a heteromultivalent recognition
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| 650 |
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4 |
|a pathological impairment
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| 650 |
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7 |
|a Amyloid beta-Peptides
|2 NLM
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| 650 |
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7 |
|a Calixarenes
|2 NLM
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| 650 |
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7 |
|a 130036-26-9
|2 NLM
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| 650 |
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7 |
|a Cyclodextrins
|2 NLM
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| 650 |
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7 |
|a amyloid beta-protein (1-42)
|2 NLM
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| 650 |
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7 |
|a Peptide Fragments
|2 NLM
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| 650 |
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7 |
|a Macrocyclic Compounds
|2 NLM
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| 700 |
1 |
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|a Xu, XinXin
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Pan, Yu-Chen
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Yan, YuXing
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Hu, Xin-Yue
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Chen, RunWen
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Ravoo, Bart Jan
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Guo, Dong-Sheng
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Zhang, Tao
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Advanced materials (Deerfield Beach, Fla.)
|d 1998
|g 33(2021), 4 vom: 01. Jan., Seite e2006483
|w (DE-627)NLM098206397
|x 1521-4095
|7 nnns
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| 773 |
1 |
8 |
|g volume:33
|g year:2021
|g number:4
|g day:01
|g month:01
|g pages:e2006483
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| 856 |
4 |
0 |
|u http://dx.doi.org/10.1002/adma.202006483
|3 Volltext
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