Aluminum and Alzheimer's disease, a personal perspective after 25 years

Perl, Daniel P.; Moalem, Sharon

doi:10.3233/jad-2006-9s332

Cited by 58 publications

(34 citation statements)

References 16 publications

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“…Aluminum (Al) is a well-known neurotoxic agent, which has been involved in neurodisorders such as Alzheimer's disease (AD) and other serious neurodegenerative diseases [1,2]. Aluminum induces the production of free radicals leading to damage in lipids, proteins, and DNA in the brain [3][4][5].…”

Section: Introductionmentioning

confidence: 99%

Role of Deferoxamine on Enzymatic Stress Markers in an Animal Model of Alzheimer’s Disease After Chronic Aluminum Exposure

Esparza

García²,

Gómez³

et al. 2010

Biol Trace Elem Res

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The effect of the chelator deferoxamine (DFO) on the activity of enzymatic stress markers was assessed in amyloid beta peptide (AβPP) transgenic mice, an animal model of Alzheimer's disease, after oral aluminum (Al) exposure for 6 months. AβPP transgenic (Tg2576) and C57BL6/SJL wild-type mice of 5 months of age were fed a diet supplemented with Al lactate (1 mg of Al/g food). Four groups of Tg2576 and wild-type animals were used: control, Al only, DFO only, and Al plus DFO. Mice in the DFO-treated groups received also subcutaneous injections of 0.20 mmol/kg/d of this chelating agent twice a week until the end of the study at 11 months of age. The hippocampus, cerebellum, and cortex were removed and processed to examine a number of oxidative stress markers. Furthermore, the expression of Cu-Zn superoxide dismutase, glutathione reductase, and catalase was evaluated by quantitative reverse transcriptase polymerase chain reaction analysis. Aluminum levels in the hippocampus of Tg2576 mice were higher than those found in cerebellum and cortex, while the main oxidative effects were evidenced in the presence of DFO only. Oral Al exposure of AβPP transgenic mice would have some potential to promote pro-oxidant events, while DFO administration would not help in preventing these deleterious effects.

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Section: Introductionmentioning

confidence: 99%

Role of Deferoxamine on Enzymatic Stress Markers in an Animal Model of Alzheimer’s Disease After Chronic Aluminum Exposure

Esparza

García²,

Gómez³

et al. 2010

Biol Trace Elem Res

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“…Increased aluminium concentrations were found in the brains of deceased Alzheimer's patients. Other studies, however, have been unable to find definite indications supporting the hypothesis that aluminium plays a causative role in Alzheimer's disease or causes pathological alterations in vivo in the species studied [14][15][16][17][18][19][20].…”

Section: Introduction and Objectivementioning

confidence: 99%

Aluminium content of selected foods and food products

Taschan²,

2011

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For many years aluminium was not considered harmful to human health because of its relatively low bioavailability. In 1965, however, animal experiments suggested a possible connection between aluminium and Alzheimer's disease. Oral intake of foodstuffs would appear to be the most important source of aluminium. Consequently, the joint FAO/WHO Expert Committee on Food Additives reduced the provisional tolerable weekly intake value for aluminium from 7 mg kg -1 body weight/week to 1 mg kg -1 body weight/week. Analysis of aluminium content of a number of foods and food products was therefore undertaken in order to evaluate the nutritional intake of aluminium. A total of 1,431 samples were analysed within the scope of this study. The data obtained allow a preliminary but current depiction of the aluminium content of selected non-animal foods, food products and beverages.

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“…Aluminium causes the accumulation of tau protein and amyloid-beta protein in experimental animals and induces neural apoptosis in vivo as well as in vitro (Kawahara, 2005). Aluminium accumulation in the tanglebearing neurons is the cause of amylotrophic lateral sclerosis and the parkinsonism-dementia complex of Guam (Perl & Moalem, 2006).…”

Section: Introductionmentioning

confidence: 98%