AustralieFrV1, Main, Exploration, bibRecord, 005824

The role of metallobiology and amyloid-β peptides in Alzheimer's disease

Identifieur interne : 005824 ( Main/Exploration ); précédent : 005823; suivant : 005825

The role of metallobiology and amyloid-β peptides in Alzheimer's disease

Auteurs : Blaine R. Roberts [Australie] ; Timothy M. Ryan [Australie] ; Ashley I. Bush [Australie] ; Colin L. Masters [Australie] ; James A. Duce [Australie]

Source :

Journal of neurochemistry [ 0022-3042 ] ; 2012.

RBID : Pascal:12-0151440

Descripteurs français

Pascal (Inist)
- Peptide, Vieillissement, Age, Réparation, Ion, Fonction cellulaire, Article synthèse, Sang, Démence d'Alzheimer, Fer, Cuivre, Pathologie de l'encéphale, Zinc, Interaction.
Wicri :
- topic : Fer, Cuivre, Zinc.

English descriptors

KwdEn :
- Age, Ageing, Alzheimer disease, Blood, Cell function, Cerebral disorder, Copper, Interaction, Ions, Iron, Peptides, Repair, Review, Zinc.

Abstract

The biggest risk factor for Alzheimer's disease is the process of ageing, but the mechanisms that lead to the manifestation of the disease remain to be elucidated. Why age triggers the disease is unclear but an emerging theme is the inability for a cell to efficiently maintain many key processes such as energy production, repair, and regenerative mechanisms. Metal ions are essential to the metabolic function of every cell. This review will explore the role and reported changes in metal ions in Alzheimer disease, particularly the brain, blood and cerebral spinal fluid, emphasizing how iron, copper and zinc may be involved through the interactions with amyloid precursor protein, the proteolytically cleaved peptide amyloid-beta (Aβ), and other related metalloproteins. Finally, we explore the monomeric makeup of possible Aβ dimers, what a dimeric Aβ species from Alzheimer's disease brain tissue is likely to be composed of, and discuss how metals may influence Aβ production and toxicity via a copper catalyzed dityrosine cross-link.

Affiliations:

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Le document en format XML

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<front><div type="abstract" xml:lang="en">The biggest risk factor for Alzheimer's disease is the process of ageing, but the mechanisms that lead to the manifestation of the disease remain to be elucidated. Why age triggers the disease is unclear but an emerging theme is the inability for a cell to efficiently maintain many key processes such as energy production, repair, and regenerative mechanisms. Metal ions are essential to the metabolic function of every cell. This review will explore the role and reported changes in metal ions in Alzheimer disease, particularly the brain, blood and cerebral spinal fluid, emphasizing how iron, copper and zinc may be involved through the interactions with amyloid precursor protein, the proteolytically cleaved peptide amyloid-beta (Aβ), and other related metalloproteins. Finally, we explore the monomeric makeup of possible Aβ dimers, what a dimeric Aβ species from Alzheimer's disease brain tissue is likely to be composed of, and discuss how metals may influence Aβ production and toxicity via a copper catalyzed dityrosine cross-link.</div>
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The role of metallobiology and amyloid-β peptides in Alzheimer's disease

The role of metallobiology and amyloid-β peptides in Alzheimer's disease

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri