Aluminium accumulation in relation to senile plaque and neurofibrillary tangle formation in the brains of patients with renal failure

Candy, J.M.; McArthur, F.K.; Oakley, Arthur E.; Taylor, Geoffrey A.; Chen, C.P.L.-H.; Mountfort, Simon A.; Thompson, J; Chalker, Paul R.; Bishop, H.E.; Beyreuther, Konrad; Perry, George; Ward, M. K.; Martyn, Christopher; Edwardson, James A.

doi:10.1016/0022-510x(92)90291-r

Cited by 74 publications

(40 citation statements)

References 29 publications

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“…The presence of aluminosilicates in plaque cores has been controversial. Some studies have reported the presence of Al [85] but this has not been confirmed by other studies [86].…”

Section: Classic and Compact Plaquesmentioning

confidence: 51%

β-Amyloid Plaques: Stages in Life History or Independent Origin?

Armstrong

1998

Dement Geriatr Cogn Disord

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Several types of discrete β-amyloid (Aβ) deposit or senile plaque have been identified in the brains of individuals with Alzheimer’s disease and Down’s syndrome. The majority of these plaques can be classified into four morphological types: diffuse, primitive, classic and compact. Two hypotheses have been proposed to account for these plaques. Firstly, that the diffuse, primitive, classic and compact plaques develop in sequence and represent stages in the life history of a single plaque type. Secondly, that the different Aβ plaques develop independently and therefore, unique factors are involved in the formation of each type. To attempt to distinguish between these hypotheses, the morphology, ultrastructure, composition, and spatial distribution in the brain of the four types of plaque were compared. Although some primitive plaques may develop from diffuse plaques, the evidence suggests that a unique combination of factors is involved in the pathogenesis of each plaque type and, therefore, supports the hypothesis that the major types of Aβ plaque develop independently.

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“…The presence of aluminosilicates in plaque cores has been controversial. Some studies have reported the presence of Al [85] but this has not been confirmed by other studies [86].…”

Section: Classic and Compact Plaquesmentioning

confidence: 51%

β-Amyloid Plaques: Stages in Life History or Independent Origin?

Armstrong

1998

Dement Geriatr Cogn Disord

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“…NFT-bearing neurons are also found after the injection of A1 salts into the brains of experimental animals (Troncoso et al, 1986;Kowall et al, 1989). NFTs are also found in patients with AD, dialysis patients with Alinduced DD (Brun and Dictor, 1981;Scholtz et al, 1987;Candy et al, 1992), and patients with parkinsonism dementidamyotropic lateral sclerosis of Guam (Per1 et al, 1982;Garmto et al, 1986), which is associated with increased brain A1 concentration. However, the location of NFT-bearing neurons in brain of these diverse Alassociated disorders differs.…”

Section: Discussionmentioning

confidence: 99%

Aluminum Enhances Iron Uptake and Expression of Neurofibrillary Tangle Protein in Neuroblastoma Cells

Abreo

Sella

et al. 1999

Journal of Neurochemistry

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Aluminum (AI) and iron (Fe) have been implicated as playing a toxic role in the pathologic lesions of Alzheimer's disease. In the following report we describe the uptake and toxicity of Al, the effect of Al on Fe uptake, and the expression of neurofibrillary tangle (NFT) protein in murine neuroblastoma cells (Neuro 2A). Significant cell Al uptake and inhibition of cell growth were seen in Neuro 2A cells at 24, 48, 72, and 96 h after plating in medium containing Al transferrin (AI-Tf) and Al citrate. Al-loaded Neuro 2A cells showed increased rates of 59Fe and lZ51-Tf uptake and total cellular Fe content at 24, 48, 72, and 96 h after plating compared with control cultures. Significant increases in NFT protein staining were detected in Al-exposed cells at 72 and 96 h in culture compared with controls.

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“…However, it has been shown that chronic exposure to Al in non-encephalopathic renal analysis patients is associated both with fibrillary deposition of ß-amyloid [11] and Alzheimer-like changes in tau protein [12]. It is not known if the increased GI absorption of Al at physiological levels of exposure seen in AD patients in the present study is paralleled by similar changes in blood-brain barrier permeability but this cannot be excluded, and the possibility of decreasing the prevalence of AD by reducing the exposure to Al in vulnerable subjects with public health measures, for example limiting Al uptake or bioavailability [20], must be considered.…”

Section: Discussionmentioning

confidence: 99%

“…Aluminium (Al) is a significant but con-troversial environmental risk factor for AD [6,7]. Evidence of Al involvement comes from several sources: the presence of alumino-silicate cores in senile plaques [8] and accumulation of Al in brain areas vulnerable in AD [9,10], the detection of immature senile plaques and Alzheimer-like changes in tau protein in postmortem brain from renal dialysis patients (with no symptoms of dialysis encephalopathy) [11,12] and the increased prevalence of AD in areas with high levels of Al in drinking water [13,14].…”

Section: Introductionmentioning

confidence: 99%

Absorption of Aluminium-26 in Alzheimer’s Disease, Measured Using Accelerator Mass Spectrometry

Moore

Day

Taylor

et al. 2000

Dement Geriatr Cogn Disord

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Although chromosomal abnormalities underpin some early onset cases of familial Alzheimer’s disease (AD), most cases are sporadic and not associated with such abnormalities. Aluminium (Al) is a significant but controversial risk factor for sporadic AD, and studies have reported associations between Al and the principal pathological features of AD, senile plaques and neurofibrillary tangles. The present study measured gastrointestinal (GI) absorption of Al under normal dietary conditions using ²⁶Al tracer and accelerator mass spectrometry (AMS). Following overnight fast, 13 AD patients (aged 63–76 years) and 13 age-matched controls (aged 62–76 years) ingested a fruit drink containing 27 ng ²⁶Al. Plasma samples were obtained before and 1 h after the drink and from these the fraction of ²⁶Al absorbed across the GI tract was estimated. The GI tract rigorously excludes Al with only 0.06–0.1% of the ingested Al being absorbed. The mean fraction absorbed by AD subjects exceeded controls by a factor of 1.64 (p≤0.05, Anova). AMS is capable of determining <10^–16 g of ²⁶Al with many orders of magnitude more sensitivity than other techniques. Using this sensitivity, we have shown, under normal physiological conditions, that the ability of the GI tract to exclude Al is reduced in AD, possibly leading to greater systemic exposure to Al. Public health measures to limit Al dietary uptake or bioavailability may decrease the prevalence of AD in the community and should be considered.

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Aluminium accumulation in relation to senile plaque and neurofibrillary tangle formation in the brains of patients with renal failure

Cited by 74 publications

References 29 publications

β-Amyloid Plaques: Stages in Life History or Independent Origin?

β-Amyloid Plaques: Stages in Life History or Independent Origin?

Aluminum Enhances Iron Uptake and Expression of Neurofibrillary Tangle Protein in Neuroblastoma Cells

Absorption of Aluminium-26 in Alzheimer’s Disease, Measured Using Accelerator Mass Spectrometry

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