Aluminum, copper, iron and zinc differentially alter amyloid-Aβ1–42 aggregation and toxicity

Fibrillation of hen egg white lysozyme triggers reduction of copper(II)

“…A recent report has revealed that metal ions such as Al(III), Fe(III) result in the formation of fibrillar aggregates in the amyloid peptide, A␤ 1-42 which was not observed in presence of Zn(II) and Cu(II) [4]. These metal ions have also been found to affect aggregation kinetics of A␤ 1-40 [6].…”

“…Recent studies demonstrate remarkable effects of Cu(II) which can either potentially promote or inhibit amyloid formation of numerous neurodegenerative disease related/unrelated proteins such as A␤-peptides, ␣-synuclein, prion protein, ubiquitin, human serum albumin, human peptide of amylin, ␤-2-microglobulin and ␤-lactoglobulin A [3][4][5][6][7][8][9][10][11][12][13]. In addition, the amyloid precursor protein (APP), A␤ 1-40 peptide, ␣-synuclein and prion (PrP) are capable of reducing Cu(II) to Cu(I) [14][15][16][17].…”

Sub-lethal levels of amyloid β-peptide oligomers decrease non-transferrin-bound iron uptake and do not potentiate iron toxicity in primary hippocampal neurons

“…We propose that under our conditions, AbOs plus Fe do not increase ryanodine receptor activity over the levels induced solely by Fe or AbOs. Yet, at longer times AbOs and Fe may act in a synergistic manner to generate oxidative stress and abnormally high calcium signals, or iron may induce the formation of different AbOs aggregates with higher toxicity (Bolognin et al 2011;Liu et al 2011). Both conditions are likely to favor cell death, as occurs progressively in the brain of AD patients where the accumulation of iron and AbOs begins many years before the diagnosis of the pathological cognitive deficit.…”

Low levels of aluminum can lead to behavioral and morphological changes associated with Alzheimer's disease and age-related neurodegeneration

“…Aluminum salts can promote Ab aggregation in vitro (Exley, 1997;Bondy and Truong, 1999;Bolognin et al, 2011), and treatment of transgenic mice over-expressing AbPP, with Al salts in the drinking water, leads to oxidative stress, Ab deposition, and plaque formation in the brain (Pratico et al, 2002). However two recent studies on Al and the promotion of Alzheimer pathology or behavior has brought this finding into question (Poirier et al, 2011;Akiyama et al, 2012).…”