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The role of metallobiology and amyloid‐β peptides in Alzheimer’s disease
Author(s) -
Roberts Blaine R.,
Ryan Timothy M.,
Bush Ashley I.,
Masters Colin L.,
Duce James A.
Publication year - 2012
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2011.07500.x
Subject(s) - disease , amyloid (mycology) , amyloid precursor protein , amyloid beta , alzheimer's disease , peptide , chemistry , neuroscience , biochemistry , microbiology and biotechnology , medicine , biology , pathology
J. Neurochem. (2012) 120 (Suppl. 1), 149–166. 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.