Aluminium and Alzheimer's Disease: Review of Possible Pathogenic Mechanisms

Armstrong, Richard A.; Winsper, S.J.; Blair, J.A.

doi:10.1159/000106845

Cited by 30 publications

(24 citation statements)

References 38 publications

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“…Much of the evidence that Al is a cause of AD is circumstantial and controversial [21]. Epidemiological studies [77,120,133] have found little correlation between environmental Al and AD.…”

Section: Aluminiummentioning

confidence: 99%

“…In addition, out of 13 studies, in which gross brain tissue has been analysed for Al, 9/13 found enhanced levels in AD brain, while 4/13 found no significant differences compared with control brains [34]. The significance of enhanced Al levels in brain is also unclear since damaged brains may accumulate Al [21]. The presence of Al may also be linked to the formation of SP and NFT.…”

Section: Aluminiummentioning

confidence: 99%

“…First, mercury can induce antibodies against renal antigens and inhibit RT6+ T-cells [107]. Second, exposure to cobalt, Al [21], tin, zirconium, and beryllium have been associated with lung inflammatory disease [63]. Lymphocyte transformation, an increase in T-cells, and the development of a granulomatous pneumonitis have been observed in these disorders [63].…”

Section: Theories Based On Immunologymentioning

confidence: 99%

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Review article What causes alzheimer’s disease?

Armstrong¹

2013

175

119

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A b s t r a c t Since the earliest descriptions of Alzheimer's disease (AD), many theories have been advanced as to its cause. These include: (1) exacerbation of aging, (2) degeneration of anatomical pathways, including the cholinergic and cortico-cortical pathways, (3) an environmental factor such as exposure to aluminium, head injury, or malnutrition, (4) genetic factors including mutations of amyloid precursor protein (APP) and presenilin (PSEN) genes and allelic variation in apolipoprotein E (Apo E), (5) mitochondrial dysfunction, (6) a compromised blood brain barrier, (7) immune system dysfunction, and (8) infectious agents. This review discusses the evidence for and against each of these theories and concludes that AD is a multifactorial disorder in which genetic and environmental risk factors interact to increase the rate of normal aging ('allostatic load'). The consequent degeneration of neurons and blood vessels results in the formation of abnormally aggregated 'reactive' proteins such as b-amyloid (Ab) and tau. Gene mutations influence the outcome of age-related neuronal degeneration to cause early onset familial AD (EO-FAD

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“…Much of the evidence that Al is a cause of AD is circumstantial and controversial [21]. Epidemiological studies [77,120,133] have found little correlation between environmental Al and AD.…”

Section: Aluminiummentioning

confidence: 99%

Section: Aluminiummentioning

confidence: 99%

Section: Theories Based On Immunologymentioning

confidence: 99%

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Review article What causes alzheimer’s disease?

Armstrong¹

2013

175

119

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“…Al was also found to be a major causative factor in the development of dialysis encephalopathy [5,6]. This element has been proposed as a contributor to the pathogenesis of serious neurological disorders such as Alzheimer's disease, amyotrophic lateral sclerosis and parkinsonism-dementia of Guam [7][8][9][10][11]. In these neurodegenerative diseases, the pathologic features that they share include abnormal phosphorylation of neuronal cytoskeletal proteins and the abnormal deposition of these proteins in neurons.…”

mentioning

confidence: 99%

Behavioral Effects of Aluminum in Mice: Influence of Restraint Stress

Colomina¹,

Sánchez²,

Sánchez-Turet³

et al. 1999

Neuropsychobiology

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The influence of restraint stress on potential aluminum (Al)-induced behavioral changes was assessed in CD-1 mice. Three groups of adult mice were given 0, 300 and 600 mg Al/kg body weight per day in drinking water for 2 weeks. One-half of the animals in each group were concurrently subjected to restraint stress during 1 h per day throughout the study. After cessation of treatment, open-field activity, active avoidance learning, and motor resistance and coordination of the animals were evaluated. At the end of the behavioral testing period, mice were killed and Al concentrations were determined in a number of tissues. There were no remarkable effects of Al, restraint stress or their combined administration on either open-field activity or on the number of avoidances in an automatic reflex conditioner. However, a lower motor resistance and coordination in a rotarod were observed following exposure to Al at 600 mg/kg/day, restraint alone or concurrent administration of Al (300 and 600 mg/kg/day) plus restraint stress. The levels of Al in whole brain and cerebellum were significantly enhanced in mice exposed to Al plus restraint. Although the present results scarcely show Al-induced neurobehavioral effects, the influence of restraint stress on Al levels in whole brain and cerebellum can be the basis for further studies on the potential role of this element in certain neurological disorders.

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“…Although aluminum certainly forms the basis of dialysis dementia, the role of this nonessential element in the etiology of Alzheimer's disease is more controversial ( 4 ). It has been claimed that chelation of aluminum with deferoxamine may ameliorate this disease (24).…”

mentioning

confidence: 99%

Active Oxygen Species Formation in Synaptosomes Exposed to an Aluminum Chelator

Bondy

Tseng

Orvig

1998

Neurotoxicology and Teratology

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Active oxygen species formation in synaptosomes exposed to an aluminum chelator. NEUROTOXICOL TERATOL 20(3) 317-320, 1998.-This study evaluates the potential of two chelators, l,2-dimethyl-3-hydroxypyridine-4-one (Hdpp) and l-n-butyl-2-methyl-3-hydroxypyridin-4-one (Hnbp ), to modulate cerebral rates of free radical production. The fluorometric assay for 2',7'-dichlorofluorescein, which is formed by oxidation of a nonfluorcscent precursor (2' .7'-dichlorofluorescin diacetate ), was used to assay reactive oxygen species (ROS) production. The chelator Hdpp alone and the aluminum complexes of each chelator, Al (dpp)i and Al (nbp),, all inhibited basal rates of generation of ROS within a rat cerebral synaptosomal fraction. In the presence of an iron salt ( 1 µ,M FeSO.). a major enhancement of synaptosomal ROS formation was apparent. However, with the addition of an cquimolar concentration of Hdpp, Al(dpp),, or Al(nbph this stimulation was completely abolished. The N-substituted-3-hydroxy-4-pyridinones have been proposed to be of clinical utility for the removal of iron or aluminum from tissues. The clinical potential of this class of chelator may be enhanced by their ability to inhibit iron-related oxidative events.

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Aluminium and Alzheimer's Disease: Review of Possible Pathogenic Mechanisms

Cited by 30 publications

References 38 publications

Review article What causes alzheimer’s disease?

Review article What causes alzheimer’s disease?

Behavioral Effects of Aluminum in Mice: Influence of Restraint Stress

Active Oxygen Species Formation in Synaptosomes Exposed to an Aluminum Chelator

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