Aluminium, Neurofibrillary Degeneration and Alzheimer's Disease

Crapper, D. R.; Krishnan, S. S.; Quittkat, S.

doi:10.1093/brain/99.1.67

Cited by 433 publications

(110 citation statements)

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“…The reported increased Al levels in the brains ofpatients with dialysis dementia (12) and Alzheimer disease (AD) (13) have led to the suggestion that Al may be an etiological agent for dementia. Other current theories to explain the pathogenesis of AD include decreased cholinergic innervation, defective protein synthesis, and a slow infectious process (14).…”

mentioning

confidence: 99%

Ferritin: isolation of aluminum-ferritin complex from brain.

Fleming

Joshi

1987

Proc. Natl. Acad. Sci. U.S.A.

136

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Ferritin was isolated from the livers and brains of two groups of rats, one of which was fed aluminum chloride (100 ,uM) for 1 year in the drinking water. Brain tissue contained about one-third ofthe amount offerritin found in the liver. While brain ferritin from normal rats contained 42.1 ± 14.3 mol of aluminum, that from the aluminum-fed group contained 115.4 ± 48.3 mol of aluminum per mol of ferritin. Liver ferritin from both groups contained similar amounts of both aluminum and iron, and the amounts were less than that found associated with brain ferritin. Ferritin isolated from the brains of patients who died of Alzheimer disease contained more aluminum and more iron than that from age-matched controls. Human brain ferritin is composed of two types of subunits-about 70% heavy chain (Mr, 22,000) and 30% light chain (Mr,19,500). The isoelectric focusing pattern of human brain ferritin was considerably different from that of human liver. Only 5 of the 20 brain ferritin bands migrated similarly to the acidic isoferritins from the liver, and the major component of brain ferritin, representing 30% of the total ferritin, had a pI of 8.0.

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mentioning

confidence: 99%

Ferritin: isolation of aluminum-ferritin complex from brain.

Fleming

Joshi

1987

Proc. Natl. Acad. Sci. U.S.A.

136

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“…Aluminum is one of the environmental factors that has been shown to be associated with both plaques and tangles in the AD brains [17], but no causal relationship has yet been proved. Formaldehyde, one of the most toxic organic compounds, has been found to induce tau to form amyloid-like aggregates [18].…”

Section: Aetiology and Pathologymentioning

confidence: 99%

Re-mention of an old neurodegenerative disease: Alzheimer’s disease

2013

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Alzheimer's disease (AD), the most common form of neuropsychiatric disorder, is characterized by neuronal degeneration and inexorably progressing dementia, especially in the elderly population. With a rapidly aging population in both developed and developing countries, AD has emerged as one of the largest growing problems worldwide. Current drugs improve the symptoms of AD, but do not have any profound intervention to delay its onset. Thus, understanding the molecular mechanisms underlying the genes tied to AD will be crucial to the development of therapeutic targets. This review will summarize the aetiology, pathology, and the evidence for the genetic components in AD, discuss the proposed amyloid cascade and the following tau hyperphosphorylation hypothesises, oxidative stress mediated neuronal cell death, as well as the function of Retromer complex during the developing of AD. Our laboratory's current research progress and the challenges that still remained will be also highlighted.

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“…Cerebral accumulation of aluminium has also been reported in several other neuro-pathological disorders including Alzheimer's disease (Good et al, 1992;Lukiw, 1997;Perl and Brondy, 1980), Down's syndrome (Crapper et al, 1973), amylotrophic lateral sclerosis (Gadjusek and Salazer, 1982;Perl et al, 1982) and the dementia of Parkinson's disease (Hirsch et al, 1991). The role of aluminium in these disorders is less clear, however high concentrations of aluminium are found in certain regions of the brains of patients with Alzheimer's disease (Kellett et al, 1986;Perl and Brody, 1980;Crapper et al, 1976;. There is also an epidemiological association between aluminium in drinking water and the incidence of Alzheimer's disease (Martyn et al, 1989).…”

Section: Introductionmentioning

confidence: 95%

The effects of aluminium and selenium supplementation on brain and liver antioxidant status in the rat

Abubakar¹,

Taylor²,

Ferns³

2004

Afr. J. Biotechnol.

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This in vivo study was designed to investigate the potential of aluminium (Al), in the absence of added iron, to participate in either antioxidant or pro-oxidant events. Some markers of oxidative stress were determined in liver and brain of rats exposed to aluminium lactate, either alone or in the presence of dietary supplements of selenium (se) as selenite. Exposure to aluminium for 21 days resulted in a statistically significant (P<0.05) decrease in brain glutathione. However, a non-significant increase in hepatic glutathione was observed in animals supplemented with either Se or Al, but Al in combination with Se prevented this elevation. In the brain a statistically non-significant increase (P>0.05) was observed in the GSH content. Contrary to what is known, Al exposure resulted in statistically significant decrease (P<0.001) in lipid peroxidation as measured by production of malondialdehyde in both liver and brain. Aluminium exposure had no significant effect on the liver and brain superoxide dismutase activity. Results of the present study suggest that in rat aluminium exposure may have both pro-oxidant and antioxidant effect. Furthermore, Se supplementation may offer some protection against aluminium toxicity but this needs to be further elucidated.

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Aluminium, Neurofibrillary Degeneration and Alzheimer's Disease

Cited by 433 publications

References 0 publications

Ferritin: isolation of aluminum-ferritin complex from brain.

Ferritin: isolation of aluminum-ferritin complex from brain.

Re-mention of an old neurodegenerative disease: Alzheimer’s disease

The effects of aluminium and selenium supplementation on brain and liver antioxidant status in the rat

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