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Titlebook: GeNeDis 2014; Neurodegeneration Panayiotis Vlamos,Athanasios Alexiou Conference proceedings 2015 The Editor(s) (if applicable) and The Auth

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發(fā)表于 2025-3-21 19:34:48 | 只看該作者 |倒序?yàn)g覽 |閱讀模式
書目名稱GeNeDis 2014
副標(biāo)題Neurodegeneration
編輯Panayiotis Vlamos,Athanasios Alexiou
視頻videohttp://file.papertrans.cn/381/380986/380986.mp4
概述Proceedings of the 1st World Congress on Geriatrics and Neurodegenerative Disease Research.Presents latest research on geriatrics, neurodegeneration and the interactions between the two.This volume fo
叢書名稱Advances in Experimental Medicine and Biology
圖書封面Titlebook: GeNeDis 2014; Neurodegeneration Panayiotis Vlamos,Athanasios Alexiou Conference proceedings 2015 The Editor(s) (if applicable) and The Auth
描述The 1st World Congress on Geriatrics and Neurodegenerative Disease Research (GeNeDis 2014), will focus on recent advances in geriatrics and neurodegeneration, ranging from basic science to clinical and pharmaceutical developments and will provide an international forum for the latest scientific discoveries, medical practices and care initiatives. Advances information technologies will be discussed along with their implications for various research, implementation and policy concerns. In addition, the conference will address European and global issues in the funding of long-term care and medico-social policies regarding elderly people. GeNeDis 2014 takes place in Corfu, Greece, 10-13 April 2014. This volume focuses on the sessions that address neurodegenerative diseases.
出版日期Conference proceedings 2015
關(guān)鍵詞bioinformatics; experimental medicine; geriatrics; neurodegeneration; neuroinformatics
版次1
doihttps://doi.org/10.1007/978-3-319-08927-0
isbn_softcover978-3-319-38197-8
isbn_ebook978-3-319-08927-0Series ISSN 0065-2598 Series E-ISSN 2214-8019
issn_series 0065-2598
copyrightThe Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerl
The information of publication is updating

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Autrement qu‘etre, ou, Au-dela de l‘essence.followed by neuronal and synapse loss, matches well with the clinical progression of AD symptomatology. Therefore, blocking the formation of NFTs is considered to be a promising approach to halt the progression of AD dementia.
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https://doi.org/10.1007/978-3-658-10780-2dant activity by using 1,1-diphenyl-2-picryl-hydrazyl and hydrogen peroxide (H.O.), and the total antioxidant capacity by a phosphomolybdenum assay. In general, the derivatives were found to exhibit antioxidant activity. Further, the compounds with dialkyl amino alkoxy at the C5 position demonstrated significant antioxidant activity.
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Die Beanspruchung der Au?enwand to identify the mechanisms causing this phenomenon and relate them with respectively computational simulations aiming to draw attention to gaps and weaknesses and possible directions for future research. The study of this phenomenon with the use of modeling techniques may be a decisive factor for its interpretation.
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Toxic Tau Aggregation in AD,followed by neuronal and synapse loss, matches well with the clinical progression of AD symptomatology. Therefore, blocking the formation of NFTs is considered to be a promising approach to halt the progression of AD dementia.
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https://doi.org/10.1007/978-3-322-91919-9nd CADASIL. This manuscript attempts to present a holistic view of the positive or negative contribution of Notch signaling in the adult brain, and at the same time to present and promote the promising research fields of study.
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