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Journal ArticleDOI

Binding studies of truncated variants of the Aβ peptide to the V-domain of the RAGE receptor reveal Aβ residues responsible for binding.

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TLDR
A truncated version of Aβ capable of blocking its receptor-mediated internalization was established, revealing the binding code and providing the lead compound in the process of drug design.
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This article is published in Biochimica et Biophysica Acta.The article was published on 2011-05-01. It has received 33 citations till now. The article focuses on the topics: RAGE (receptor) & Binding domain.

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Journal ArticleDOI

The role of advanced glycation end products in various types of neurodegenerative disease: a therapeutic approach

TL;DR: Several new therapeutic approaches that have been applied to treat these devastating disorders, including the use of various synthetic and naturally occurring inhibitors are discussed, including modulation of the AGE-RAGE axis is considered promising in the prevention of neurodegenerative diseases.
Journal ArticleDOI

Molecular strategies to prevent, inhibit, and degrade advanced glycoxidation and advanced lipoxidation end products

TL;DR: The review discusses inhibitors of ALE and AGE formation, cross-link breakers, ALE/AGE elimination by enzymes and proteolytic systems, receptors for advanced glycation end products (RAGEs) and blockade of the ligand–RAGE axis.
Book ChapterDOI

RAGE-mediated cell signaling.

TL;DR: RAGE (receptor for advanced glycation end products) is a multi-ligand receptor that belongs to the immunoglobulin superfamily of transmembrane proteins and has been mainly studied as a pathogenetic factor of several diseases.
Journal ArticleDOI

Microenvironment Remodeling Micelles for Alzheimer's Disease Therapy by Early Modulation of Activated Microglia

TL;DR: The results indicate that microglia can be exploited as an early target for AD treatment and their states can be controlled via microenvironment modulation.
Journal ArticleDOI

Is RAGE still a therapeutic target for Alzheimer’s disease?

TL;DR: Despite recent setbacks in the development of RAGE-based therapies for AD, a new generation of compounds that regulate RAGE activity could be efficacious and careful studies are needed to ensure safety and efficacy in chronic treatment before clinical trials.
References
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Journal ArticleDOI

Alzheimer's disease: the amyloid cascade hypothesis

TL;DR: An extensive catalog of genes that act in a migrating cell is provided, unique molecular functions involved in nematode cell migration are identified, and similar functions in humans are suggested.
Journal ArticleDOI

Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid beta-peptide.

TL;DR: Findings in other neurodegenerative diseases indicate that a broadly similar process of neuronal dysfunction is induced by diffusible oligomers of misfolded proteins.
Journal ArticleDOI

Naturally secreted oligomers of amyloid beta protein potently inhibit hippocampal long-term potentiation in vivo.

TL;DR: It is reported that natural oligomers of human Aβ are formed soon after generation of the peptide within specific intracellular vesicles and are subsequently secreted from the cell, indicating that synaptotoxic Aβ oligomers can be targeted therapeutically.
Book

Proteins: Structures and Molecular Properties

TL;DR: This paper discusses the physical properties of polypeptides, the structure of which has been determined Crystallographically to High Resolution and its role in the biosynthesis of Proteins.
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