Amyloid Beta and Tau Proteins as Therapeutic Targets for Alzheimer’s Disease Treatment: Rethinking the Current Strategy
Author(s) -
Siddhartha MondragónRodríguez,
George Perry,
Xiongwei Zhu,
Jannic Boehm
Publication year - 2012
Publication title -
international journal of alzheimer s disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.657
H-Index - 49
eISSN - 2090-8024
pISSN - 2090-0252
DOI - 10.1155/2012/630182
Subject(s) - medicine , disease , amyloid (mycology) , amyloid beta , alzheimer's disease , current (fluid) , beta (programming language) , bioinformatics , neuroscience , pathology , psychology , computer science , biology , electrical engineering , programming language , engineering
Alzheimer's disease (AD) is defined by the concurrence of accumulation of abnormal aggregates composed of two proteins: Amyloid beta (A β ) 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 A β 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.
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