Gastrointestinal Absorption of Aluminium in Alzheimer's Disease: Response to Aluminium Citrate

Taylor, Geoffrey A.; Ferrier, I. Nicol; McLoughlin, I J; Fairbairn, Andrew; McKeith, Ian G.; Lett, Debra J.; Edwardson, James A.

doi:10.1093/ageing/21.2.81

Cited by 66 publications

(34 citation statements)

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“…Our findings agree with the hypothesis that a chronic lowgrade aluminum intoxication plays a role in the development not only of Alzheimer's disease but also of bone fragility: the greater the aluminum exposure, the higher the risk of an early fracture. This would explain the higher aluminum content in younger hipfracture patients in our study-otherwise unexpected because aluminum absorption increases with age (Taylor et al 1992)-as well as the increased risk of fragility fractures in patients with Alzheimer's disease (Leitch et al 1964, Hansson et al 1982. However, the relationship between aluminum accumulation (as measured in the bone) and Alzheimer's disease cannot be a simple one, as not all cases with high aluminum content result in Alzheimer's disease (Figure).…”

Section: Commentsmentioning

confidence: 65%

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Aluminum, Alzheimer's disease and bone fragility

Mjöberg

Hellquist

Mallmin

et al. 1997

Acta Orthopaedica Scandinavica

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Section: Commentsmentioning

confidence: 65%

“…The aluminum absorption varies largely between individuals, increases with age and is raised in young patients with Alzheimer's disease (Taylor et al 1992). Most resorbed aluminum is excreted; the non-excreted part is largely deposited in bone.…”

mentioning

confidence: 99%

Aluminum, Alzheimer's disease and bone fragility

Mjöberg

Hellquist

Mallmin

et al. 1997

Acta Orthopaedica Scandinavica

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“…When aluminum is only regulated as a water quality nuisance, only fluoride is considered for its potential health effects. Too narrow a focus on fluoride artificially limits populations at risk to those with compromised fluoride excretion (renal insufficiency), excluding those with higher than normal aluminum absorption (e.g., the elderly, Alzheimer and Down's syndrome patients 83,84 ). This shortsighted exclusion is avoidable if drinking water regulations addressed exposures to Al-fluoride complexes in addition to individual aluminum or fluoride levels.…”

Section: Mullenix Metal Contaminants Of Raw Fluoride Additivesmentioning

confidence: 99%

A new perspective on metals and other contaminants in fluoridation chemicals

Mullenix

2014

International Journal of Occupational and Environmental Health

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Background: Fluoride additives contain metal contaminants that must be diluted to meet drinking water regulations. However, each raw additive batch supplied to water facilities does not come labeled with concentrations per contaminant. This omission distorts exposure profiles and the risks associated with accidents and routine use. Objectives: This study provides an independent determination of the metal content of raw fluoride products. Methods: Metal concentrations were analyzed in three hydrofluorosilicic acid (HFS) and four sodium fluoride (NaF) samples using inductively coupled plasma-atomic emission spectrometry. Arsenic levels were confirmed using graphite furnace atomic absorption analysis. Results: Results show that metal content varies with batch, and all HFS samples contained arsenic (4.9-56.0 ppm) or arsenic in addition to lead (10.3 ppm). Two NaF samples contained barium (13.3-18.0 ppm) instead. All HFS (212-415 ppm) and NaF (3312-3630 ppm) additives contained a surprising amount of aluminum. Conclusions: Such contaminant content creates a regulatory blind spot that jeopardizes any safe use of fluoride additives.

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“…The role of citrate and ascorbate in promoting absorption and excretion of Al, awaits clarification (Doming0 et al 1991). Absorption of aluminium citrate in humans increases with age, and in younger A D subjects compared with age-matched controls (Taylor et al 1992). …”

Section: Toxico-dieteticsmentioning

confidence: 99%

Nutrient and toxin interactions in neurodegenerative disease

Evans

1994

Proc. Nutr. Soc.

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The brain is the most complex organ of the body. Its effective function is dependent on its unique anatomical structure and neuronal cell morphology, together with the efficient coordination of its metabolic and physiological processes. The degenerative diseases of the brain, for example Huntington's, Parkinson's and Alzheimer's disease (AD), are generally characterized by an associated loss of functional neurones, with accompanying motor, memory and cognitive deficits.In the case of familial amyotrophic lateral sclerosis (ALS; Deng et al. 1993), Huntington's disease, early-onset dementia of familial AD (Martin, 1993), and the prion diseases (the spongiform encephalopathies, i.e. Creutzfeldt-Jacob disease and the Gerstmann-Straussler-Scheinker syndrome; Prusiner, 1991), a genetic aetiology has been demonstrated. The larger number of so-called sporadic cases of AD which occur in the 8th and 9th decades of life, suggests that environmental factors are also operative. Even so, recent findings concerning apolipoprotein E €4 allele indicate genetic polymorphisms are significant risk factors in the development of late-onset AD as well . Hence, senile dementia of the Alzheimer type, the most common of the neurodegenerative diseases, appears to be of multifactorial origin, presenting a complex interplay of genetic, environmental, and age-related factors (Calne et al. 1986). B R A I N R E S E A R C HUndertaking studies into the toxicological and nutritional aspects of neurodegeneration, poses a range of ethical, organizational, technical and financial, challenges. Since there is no laboratory test for AD and the definitive diagnosis is dependent on postmortem identification and quantification of the pathognomic intracellular neurofibrillary tangles and extracellular senile plaques within the brain, epidemiological and clinical investigations into AD are extremely problematic. However, tests for cognitive function, and development of new in vivo imaging techniques, namely magnetic resonance imaging and positron emission topography scans, do permit a degree of clinical assessment.The inherent difficulty of research into the brain is compounded not only by the diverse range of neuronal and glial cell types and the complexity of the integrated neural network, but also by the properties of redundancy and plasticity exhibited by the brain. Brain damage related to degenerative change may not become apparent until the loss of neurones reaches a particular threshold level. Hence, cognitive deficits appearing in later life may not be directly caused by senility or the ageing process itself, but may be the result of developmental deficits or toxic damage which has occurred several decades earlier. Studies indicating the major significance of pre-or early postnatal nutrition to infant brain development (Lucas, 1993) and the subsequent development of disease in adult life (Barker et al. 1989), are of particular importance in relation to the nonreplicative nature of neuronal cells. While the significance of proper nutrition in early b...

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Gastrointestinal Absorption of Aluminium in Alzheimer's Disease: Response to Aluminium Citrate

Cited by 66 publications

References 0 publications

Aluminum, Alzheimer's disease and bone fragility

Aluminum, Alzheimer's disease and bone fragility

A new perspective on metals and other contaminants in fluoridation chemicals

Nutrient and toxin interactions in neurodegenerative disease

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