Aluminosilicates and the Ageing Brain: Implications for the Pathogenesis of Alzheimer's Disease

Edwardson, J. A.; Klinowski, Jacek; Oakley, Arthur E.; Perry, Robert H.; Candy, J.

doi:10.1002/9780470513323.ch10

Cited by 16 publications

(8 citation statements)

References 23 publications

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“…Additionally, Al is also linked to other pathologies such as dialysis dementia, microcytic anemia, osteomalacia, and epilepsy (30). Our laboratory studies (66,71) have also shown that Al exposure causes neuropathological (Figure 1), neurobehavioral, and neurochemical changes resulting in impaired learning ability.…”

Section: Al Induced Symptoms Mimic Ad Symptomsmentioning

confidence: 66%

Understanding Aspects of Aluminum Exposure in Alzheimer's Disease Development

et al. 2015

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Aluminum is a ubiquitously abundant nonessential element. Aluminum has been associated with neurodegenerative diseases such as Alzheimer's disease (AD), amyotrophic lateral sclerosis, and dialysis encephalopathy. Many continue to regard aluminum as controversial although increasing evidence supports the implications of aluminum in the pathogenesis of AD. Aluminum causes the accumulation of tau protein and Aβ protein in the brain of experimental animals. Aluminum induces neuronal apoptosis in vivo and in vitro, either by endoplasmic stress from the unfolded protein response, by mitochondrial dysfunction, or a combination of them. Some, people who are exposed chronically to aluminum, either from through water and/or food, have not shown any AD pathology, apparently because their gastrointestinal barrier is more effective. This article is written keeping in mind mechanisms of action of aluminum neurotoxicity with respect to AD.

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Section: Al Induced Symptoms Mimic Ad Symptomsmentioning

confidence: 66%

Understanding Aspects of Aluminum Exposure in Alzheimer's Disease Development

et al. 2015

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“…The presence of Al in the cores of senile plaques has been controversial for a long time [18][19][20][21][22][23]. One of the reasons may be that Al in amyloid fibers in the core could not be stained histochemically [10], while Al in the neurofibrillary tangles and nuclei of nerve cells in the AD brain is stained clearly by histochemistry [8][9][10].…”

Section: Discussionmentioning

confidence: 99%

“…Landsberg et al also failed to demonstrate the presence of Al in senile plaque cores by microprobe PIXE analysis [22]. They concluded that the Al previously detected in isolated senile plaque cores [18,19] was the result of contamination by Al silicates, which were the main components of the dust in the air. On the other hand, Beauchemin and Kisilevsky detected Al in isolated senile plaques cores from the AD brain using inductively coupled plasma mass spectrometry [23].…”

Section: Introductionmentioning

confidence: 99%

“…In 1986, Edwardson et al measured high concentrations of Al (4-19%) and silicon (Si; 6-24%) in the isolated cores of senile plaques using energy-dispersive X-ray spectroscopy (EDX) combined with scanning electron microscopy (SEM-EDX) [18,19], whereas Jacobs et al and Tokutake et al failed to detect Al in senile plaques in the AD brain by SEM-EDX [20,21]. Landsberg et al also failed to demonstrate the presence of Al in senile plaque cores by microprobe PIXE analysis [22].…”

Section: Introductionmentioning

confidence: 99%

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Demonstration of aluminum in amyloid fibers in the cores of senile plaques in the brains of patients with Alzheimer’s disease

Yumoto¹,

Kakimi

Ohsaki

et al. 2009

Journal of Inorganic Biochemistry

146

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“…The presence of Al may also be linked to the formation of SP and NFT. Studies have either reported [61], or not reported [109], Al in association with the cores of classic Ab deposits, but it is not clear whether this type of SP is especially frequent in AD [18]. Al has also been detected in pyramidal neurons containing NFT [142,143].…”

Section: Aluminiummentioning

confidence: 99%

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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Aluminosilicates and the Ageing Brain: Implications for the Pathogenesis of Alzheimer's Disease

Cited by 16 publications

References 23 publications

Understanding Aspects of Aluminum Exposure in Alzheimer's Disease Development

Understanding Aspects of Aluminum Exposure in Alzheimer's Disease Development

Demonstration of aluminum in amyloid fibers in the cores of senile plaques in the brains of patients with Alzheimer’s disease

Review article What causes alzheimer’s disease?

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