Amyloid Beta and Tau Proteins as Therapeutic Targets for Alzheimer’s Disease Treatment: Rethinking the Current Strategy

Amyloid Beta and Tau Proteins as Therapeutic Targets for Alzheimer’s Disease Treatment: Rethinking the Current Strategy

Alzheimer’s disease (AD) is defined by the concurrence of accumulation of abnormal aggregates composed of two proteins: Amyloid beta (Aβ) and tau, and of cellular changes including neurite degeneration and loss of neurons and cognitive functions. Based on their strong association with disease, genet...

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Main Authors: Siddhartha Mondragón-Rodríguez, George Perry, Xiongwei Zhu, Jannic Boehm
Format: Article
Language:English
Published: Hindawi Limited 2012-01-01
Series:International Journal of Alzheimer's Disease
Online Access:http://dx.doi.org/10.1155/2012/630182
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spelling doaj-638414c97a7e4465aeba84a4da2054f22020-11-24T23:41:27ZengHindawi LimitedInternational Journal of Alzheimer's Disease2090-80242090-02522012-01-01201210.1155/2012/630182630182Amyloid Beta and Tau Proteins as Therapeutic Targets for Alzheimer’s Disease Treatment: Rethinking the Current StrategySiddhartha Mondragón-Rodríguez0George Perry1Xiongwei Zhu2Jannic Boehm3Le Groupe de Recherche sur le Système Nerveux Central, Département de Physiologie, Université de Montréal, Montréal, QC, CanadaUTSA Neurosciences Institute and Department of Biology, College of Sciences, University of Texas at San Antonio, San Antonio, TX, USADepartment of Pathology, Case Western Reserve University, Cleveland, OH, USALe Groupe de Recherche sur le Système Nerveux Central, Département de Physiologie, Université de Montréal, Montréal, QC, CanadaAlzheimer’s disease (AD) is defined by the concurrence of accumulation of abnormal aggregates composed of two proteins: Amyloid beta (Aβ) and tau, and of cellular changes including neurite degeneration and loss of neurons and cognitive functions. Based on their strong association with disease, genetically and pathologically, it is not surprising that there has been a focus towards developing therapies against the aggregated structures. Unfortunately, current therapies have but mild benefit. With this in mind we will focus on the relationship of synaptic plasticity with Aβ and tau protein and their role as potential targets for the development of therapeutic drugs. Finally, we will provide perspectives in developing a multifactorial strategy for AD treatment.http://dx.doi.org/10.1155/2012/630182
collection DOAJ
language English
format Article
sources DOAJ
author Siddhartha Mondragón-Rodríguez
George Perry
Xiongwei Zhu
Jannic Boehm
spellingShingle Siddhartha Mondragón-Rodríguez
George Perry
Xiongwei Zhu
Jannic Boehm
Amyloid Beta and Tau Proteins as Therapeutic Targets for Alzheimer’s Disease Treatment: Rethinking the Current Strategy
International Journal of Alzheimer's Disease
author_facet Siddhartha Mondragón-Rodríguez
George Perry
Xiongwei Zhu
Jannic Boehm
author_sort Siddhartha Mondragón-Rodríguez
title Amyloid Beta and Tau Proteins as Therapeutic Targets for Alzheimer’s Disease Treatment: Rethinking the Current Strategy
title_short Amyloid Beta and Tau Proteins as Therapeutic Targets for Alzheimer’s Disease Treatment: Rethinking the Current Strategy
title_full Amyloid Beta and Tau Proteins as Therapeutic Targets for Alzheimer’s Disease Treatment: Rethinking the Current Strategy
title_fullStr Amyloid Beta and Tau Proteins as Therapeutic Targets for Alzheimer’s Disease Treatment: Rethinking the Current Strategy
title_full_unstemmed Amyloid Beta and Tau Proteins as Therapeutic Targets for Alzheimer’s Disease Treatment: Rethinking the Current Strategy
title_sort amyloid beta and tau proteins as therapeutic targets for alzheimer’s disease treatment: rethinking the current strategy
publisher Hindawi Limited
series International Journal of Alzheimer's Disease
issn 2090-8024
2090-0252
publishDate 2012-01-01
description Alzheimer’s disease (AD) is defined by the concurrence of accumulation of abnormal aggregates composed of two proteins: Amyloid beta (Aβ) and tau, and of cellular changes including neurite degeneration and loss of neurons and cognitive functions. Based on their strong association with disease, genetically and pathologically, it is not surprising that there has been a focus towards developing therapies against the aggregated structures. Unfortunately, current therapies have but mild benefit. With this in mind we will focus on the relationship of synaptic plasticity with Aβ and tau protein and their role as potential targets for the development of therapeutic drugs. Finally, we will provide perspectives in developing a multifactorial strategy for AD treatment.
url http://dx.doi.org/10.1155/2012/630182
work_keys_str_mv AT siddharthamondragonrodriguez amyloidbetaandtauproteinsastherapeutictargetsforalzheimersdiseasetreatmentrethinkingthecurrentstrategy
AT georgeperry amyloidbetaandtauproteinsastherapeutictargetsforalzheimersdiseasetreatmentrethinkingthecurrentstrategy
AT xiongweizhu amyloidbetaandtauproteinsastherapeutictargetsforalzheimersdiseasetreatmentrethinkingthecurrentstrategy
AT jannicboehm amyloidbetaandtauproteinsastherapeutictargetsforalzheimersdiseasetreatmentrethinkingthecurrentstrategy
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