Involvement of altered cytoskeletal protein phosphorylation in aluminum-induced CNS dysfunction

Julka, Deepinder; Gill, Kirandip

doi:10.1002/(sici)1522-7146(1996)11:5<227::aid-jbt3>3.0.co;2-m

Cited by 5 publications

(8 citation statements)

References 29 publications

(30 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…From these reports, it can be concluded that hippocampus which is the seat of memory and learning is the most affected region of the brain. Decrease in the Bmax value suggests that there is a decrease in the number of receptors in hippocampus, implying that a decreased transmission of nerve impulses may be responsible for neurobehavioral alterations (64,65,67). A similar decrease in the number of receptors can be responsible for the state of dementia, as observed in patients with AD (92).…”

Section: Al Exposure and Neurobehavioral Changessupporting

confidence: 53%

“…Based on earlier reports from our laboratory (64,65,67), it has been shown that following chronic and subacute exposure to Al, male wistar rats showed maximum accumulation of Al in hippocampus.…”

Section: Al Exposure and Neurobehavioral Changesmentioning

confidence: 99%

“…Our data also revealed a significant retardation in the retention of the learned task in the Al-exposed group compared to the control group. Hippocampal damage has been correlated with significantly decreased performance during memory function tests in experimental animals (64,65,67,109,113). The possibility that altered motor function could influence the changes in the memory tasks could be ruled out, as no significant changes in the spontaneous locomotor activity and rota rod tests were observed.…”

Section: Al Exposure and Neurobehavioral Changesmentioning

confidence: 99%

See 2 more Smart Citations

Understanding Aspects of Aluminum Exposure in Alzheimer's Disease Development

et al. 2015

View full text Add to dashboard Cite

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.

show abstract

Section: Al Exposure and Neurobehavioral Changessupporting

confidence: 53%

Section: Al Exposure and Neurobehavioral Changesmentioning

confidence: 99%

Section: Al Exposure and Neurobehavioral Changesmentioning

confidence: 99%

See 1 more Smart Citation

Understanding Aspects of Aluminum Exposure in Alzheimer's Disease Development

et al. 2015

View full text Add to dashboard Cite

show abstract

“…[43] Accelerates phosphorylation and accumulation of neurofilament. [44] Enhances Ca 2+ /Calmodulin dependent protein kinase activity. [45] Accelerates phosphorylation of MAP 2 and neurofilament.…”

Section: Phosphorylation and Dephosphorylationmentioning

confidence: 99%

Aluminium and Other Metals May Pose a Risk to Children with Autism Spectrum Disorder: Biochemical and Behavioural Impairments

Melendez¹

2013

Clin Exp Pharmacol

View full text Add to dashboard Cite

Recent studies have shown that some toxic metals have been associated with neurological diseases. The binding and transport of these metals in the blood may occur by species of High Molecular Mass (HMM) and Low Molecular Weight Species (LMM) of proteins. These main species are known to be responsible for aluminum transporting is the case of transferrin and citrate. It seems that autistic children may have a genetic predisposition to accumulate large amounts of metals as it is has been proposed. This study seeks to understand the toxic mechanism of selected metals in autistic children and its correlation with the psycho-metabolic implications of the syndrome. Preliminary results have indicated that some metals such as chromium, arsenic and particularly aluminum were elevated in the blood of an autistic child, as compared to reference values of a normal child. A case-control study is under investigation. Furthermore, the consequences of the disease, as such the difficulties in socialization and language skill disabilities may also be related to the burden of toxic metals in general, particularly aluminum.

show abstract

“…One article [160] has disputed the original report [161] that Al binds to spin-labeled CaM. However, Al-CaM interactions have since been confirmed by many techniques including the use of steady-state and timedependent fluorescence spectroscopy, circular dicroic spectroscopy, equilibrium dialysis, electron paramagnetic resonance, heteronuclear 2-dimensional NMR, surface plasma resonance, calorimetry, monoclonal antibody (non)recognition and by chelation studies using citric acid or desferrioxamine B which can both chelate Al and reverse the effects of Al on CaM conformational change that occurs with Al exposure [157,159,[162][163][164][165][166][167][168][169]. These studies and others have helped to define conditions under which Al binds to CaM, and how Al interferes with signal transduction.…”

Section: Al Alters Cam and Cam-mediated Signal Transduction In Neuralmentioning

confidence: 99%

Aluminum Disruption of Calcium Homeostasis and Signal Transduction Resembles Change that Occurs in Aging and Alzheimer's Disease

Walton

2012

JAD

View full text Add to dashboard Cite

Most humans living in industrialized societies are routinely exposed to bioavailable aluminum salts in the form of additives-in commercially-prepared foods, alum-clarified drinking water, certain pharmaceuticals, sunscreens, and other topical applications. Minute amounts of this aluminum are absorbed into the circulation. Trace aluminum levels cross the blood-brain barrier and progressively accumulate in large pyramidal neurons of the hippocampus, cortex, and other brain regions vulnerable in Alzheimer's disease. More aluminum enters the brain than leaves, resulting in a net increase in intraneuronal aluminum with advancing age. Aluminum is responsible for two main types of toxic damage in cells. As a pro-oxidant, aluminum causes oxidative damage both on its own and in synergy with iron. Aluminum also competes with, and substitutes for, essential metals-primarily Mg2+, iron and Ca2+ ions-in or on proteins and their co-factors. The author hypothesizes that intraneuronal aluminum interferes with Ca2+ metabolism in the aged brain and describes a way to test this hypothesis. This paper reviews: 1) major changes that occur in brain Ca2+ homeostasis and Ca2+ signaling, subtly with aging and more overtly in Alzheimer's disease; and 2) evidence from the scientific literature that aluminum causes these same changes in neurons.

show abstract

Involvement of altered cytoskeletal protein phosphorylation in aluminum-induced CNS dysfunction

Cited by 5 publications

References 29 publications

Understanding Aspects of Aluminum Exposure in Alzheimer's Disease Development

Understanding Aspects of Aluminum Exposure in Alzheimer's Disease Development

Aluminium and Other Metals May Pose a Risk to Children with Autism Spectrum Disorder: Biochemical and Behavioural Impairments

Aluminum Disruption of Calcium Homeostasis and Signal Transduction Resembles Change that Occurs in Aging and Alzheimer's Disease

Contact Info

Product

Resources

About