Effects of oral aluminum exposure on behavior and neurogenesis in a transgenic mouse model of Alzheimer's disease

Ribes, Diana; Colomina, María Teresa; Vicens, Paloma; Domingo, José L.

doi:10.1016/j.expneurol.2008.08.017

Cited by 86 publications

(42 citation statements)

References 55 publications

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“…It is characterized by excessive production and accumulation of Ab peptide, the pathological product of amyloid precursor protein (APP) by sequential proteolytic action of b-and c-secretases [1]. Aluminum (Al) is the third most abundant metal in the earth's crust and its role in the etiology and pathogenesis of AD has drawn more perceive, due to the well documented animal experiments [2] and clinical studies [3]. It is reported that Al is known to accelerate extracellular Ab generation and aggregation [4,5].…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Neuroprotective Effect of Hesperidin on Aluminium Chloride Induced Alzheimer’s Disease in Wistar Rats

et al. 2015

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The present study was aimed to evaluate the protective effect of hesperidin (Hes) on aluminium chloride (AlCl3) induced neurobehavioral and pathological changes in Alzheimeric rats. Intraperitonial injection of AlCl3 (100 mg/kg body weight) for 60 days significantly elevated the levels of aluminium (Al), activity of acetylcholinesterase (AChE) and protein expressions of amyloid precursor protein (APP), β amyloid (Aβ 1-42), β and γ secretases as compared to control group in hippocampus and cortex of rat brain. Hes administration orally along with AlCl3 injection for 60 days, significantly revert the Al concentration, AChE activity and Aβ synthesis-related molecules in the studied brain regions. Our results showed that aluminum exposure was significantly reduced the spontaneous locomotor and exploratory activities in open field test and enhanced the learning and memory impairments in morris water maze test. The behavioral impairments caused by aluminum were significantly attenuated by Hes. The histopathological studies in the hippocampus and cortex of rat brain also supported that Hes (100 mg/kg) markedly reduced the toxicity of AlCl3 and preserved the normal histoarchitecture pattern of the hippocampus and cortex. From these results, it is concluded that hesperidin can reverse memory loss caused by aluminum intoxication through attenuating AChE activity and amyloidogenic pathway.

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Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Neuroprotective Effect of Hesperidin on Aluminium Chloride Induced Alzheimer’s Disease in Wistar Rats

et al. 2015

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“…This mouse is currently considered as an experimental model of AD (Chapman et al, 1999;Pratico et al, 2002;Rodrigo et al, 2004;Maynard et al, 2006;López-Toledano andShelanski, 2007, Duyckaerts et al, 2008). Only results of a few studies concerning Al effects in these animals have been reported (Pratico et al, 2002;Drago et al, 2008;Gómez et al, 2008;Ribes et al, 2008). In relation to it, Pratico et al (2002) studied in Tg2576 mice the effects of dietary Al administration (2 mg of Al/kg of diet).…”

Section: Introductionmentioning

confidence: 99%

Oxidative stress status and RNA expression in hippocampus of an animal model of Alzheimer's disease after chronic exposure to aluminum

et al. 2009

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It is well established that aluminum (Al) is a neurotoxic agent that induces the production of free radicals in brain. Accumulation of free radicals may cause degenerative events of aging such as Alzheimer's disease. On the other hand, melatonin (Mel) is a known antioxidant, which can directly act as free radical scavenger, or indirectly by inducing the expression of some genes linked to the antioxidant defense. In this study, AbetaPP female transgenic (Tg2576) (Tg) and wild-type mice (5 months of age) were fed with Al lactate supplemented in the diet (1 mg Al/g diet). Simultaneously, animals received oral Mel (10 mg/kg) dissolved in tap water until the end of the study at 11 months of age. Four treatment groups were included for both Tg and wild-type mice: control, Al only, Mel only, and Al+Mel. At the end of the period of treatment, hippocampus was removed and processed to examine the following oxidative stress markers: reduced glutathione (GSH), oxidized glutathione (GSSG), superoxide dismutase (SOD), glutathione reductase (GR), glutathione peroxidase (GPx), catalase (CAT), and thiobarbituric acid reactive substances (TBARS). Moreover, the gene expression of Cu-ZnSOD, GR, and CAT was evaluated by real-time RT-PCR. Aluminum concentration in hippocampus was also determined. The biochemical changes observed in this tissue suggest that Al acts as a pro-oxidant agent. Melatonin exerts an antioxidant action by increasing the mRNA levels of the antioxidant enzymes SOD, CAT, and GR evaluated in presence of Al and Mel, with independence of the animal model.

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“…In the past 3 decades, accumulating evidence has suggested that exposure to a high level of aluminium (Al) leads to neurofibrillary degeneration, and that Al concentration is increased in degenerating neurons in AD [2] . The role of Al in the etiology and pathogenesis of AD has drawn more attention, due to the well documented Al-induced cognitive impairment from clinical observations [3] and animal experiments [4] . The amyloid cascade hypothesis proposes that accumulation of Aβ derived from proteolytic cleavage of amyloid precursor protein (APP) in the brain is the primary stimulator for AD pathogenesis [5] .…”

Section: Introductionmentioning

confidence: 99%

Tetrahydroxy stilbene glucoside reduces the cognitive impairment and overexpression of amyloid precursor protein induced by aluminum exposure

Luo¹,

Yang²,

Shi³

et al. 2009

Neurosci. Bull.

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Effects of oral aluminum exposure on behavior and neurogenesis in a transgenic mouse model of Alzheimer's disease

Cited by 86 publications

References 55 publications

RETRACTED ARTICLE: Neuroprotective Effect of Hesperidin on Aluminium Chloride Induced Alzheimer’s Disease in Wistar Rats

RETRACTED ARTICLE: Neuroprotective Effect of Hesperidin on Aluminium Chloride Induced Alzheimer’s Disease in Wistar Rats

Oxidative stress status and RNA expression in hippocampus of an animal model of Alzheimer's disease after chronic exposure to aluminum

Tetrahydroxy stilbene glucoside reduces the cognitive impairment and overexpression of amyloid precursor protein induced by aluminum exposure

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