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Molecular Targets in Alzheimer's Disease: From Pathogenesis to Therapeutics

Alzheimer's disease (AD) is characterized by progressive cognitive decline usually beginning with impairment in the ability to form recent memories. Nonavailability of definitive therapeutic strategy urges developing pharmacological targets based on cell signaling pathways. A great revival of i...

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Detalles Bibliográficos
Autores principales: Cheng, Xuan, Zhang, Lu, Lian, Ya-Jun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4668300/
https://www.ncbi.nlm.nih.gov/pubmed/26665008
http://dx.doi.org/10.1155/2015/760758
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author Cheng, Xuan
Zhang, Lu
Lian, Ya-Jun
author_facet Cheng, Xuan
Zhang, Lu
Lian, Ya-Jun
author_sort Cheng, Xuan
collection PubMed
description Alzheimer's disease (AD) is characterized by progressive cognitive decline usually beginning with impairment in the ability to form recent memories. Nonavailability of definitive therapeutic strategy urges developing pharmacological targets based on cell signaling pathways. A great revival of interest in nutraceuticals and adjuvant therapy has been put forward. Tea polyphenols for their multiple health benefits have also attracted the attention of researchers. Tea catechins showed enough potentiality to be used in future as therapeutic targets to provide neuroprotection against AD. This review attempts to present a concise map of different receptor signaling pathways associated with AD with an insight into drug designing based on the proposed signaling pathways, molecular mechanistic details of AD pathogenesis, and a scientific rationale for using tea polyphenols as proposed therapeutic agents in AD.
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spelling pubmed-46683002015-12-10 Molecular Targets in Alzheimer's Disease: From Pathogenesis to Therapeutics Cheng, Xuan Zhang, Lu Lian, Ya-Jun Biomed Res Int Review Article Alzheimer's disease (AD) is characterized by progressive cognitive decline usually beginning with impairment in the ability to form recent memories. Nonavailability of definitive therapeutic strategy urges developing pharmacological targets based on cell signaling pathways. A great revival of interest in nutraceuticals and adjuvant therapy has been put forward. Tea polyphenols for their multiple health benefits have also attracted the attention of researchers. Tea catechins showed enough potentiality to be used in future as therapeutic targets to provide neuroprotection against AD. This review attempts to present a concise map of different receptor signaling pathways associated with AD with an insight into drug designing based on the proposed signaling pathways, molecular mechanistic details of AD pathogenesis, and a scientific rationale for using tea polyphenols as proposed therapeutic agents in AD. Hindawi Publishing Corporation 2015 2015-11-19 /pmc/articles/PMC4668300/ /pubmed/26665008 http://dx.doi.org/10.1155/2015/760758 Text en Copyright © 2015 Xuan Cheng et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Cheng, Xuan
Zhang, Lu
Lian, Ya-Jun
Molecular Targets in Alzheimer's Disease: From Pathogenesis to Therapeutics
title Molecular Targets in Alzheimer's Disease: From Pathogenesis to Therapeutics
title_full Molecular Targets in Alzheimer's Disease: From Pathogenesis to Therapeutics
title_fullStr Molecular Targets in Alzheimer's Disease: From Pathogenesis to Therapeutics
title_full_unstemmed Molecular Targets in Alzheimer's Disease: From Pathogenesis to Therapeutics
title_short Molecular Targets in Alzheimer's Disease: From Pathogenesis to Therapeutics
title_sort molecular targets in alzheimer's disease: from pathogenesis to therapeutics
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4668300/
https://www.ncbi.nlm.nih.gov/pubmed/26665008
http://dx.doi.org/10.1155/2015/760758
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