Hemodynamic and Neuropathological Analysis in Rats with Aluminum Trichloride-Induced Alzheimer's Disease

Chen, Szu-Ming; Fan, Chi-Chen; Chiue, Ming-Shiuan; Chou, Chi; Chen, Jyh-Horng; Hseu, Ruey‐Shyang

doi:10.1371/journal.pone.0082561

Cited by 22 publications

(21 citation statements)

References 55 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…4). This could be as a result of relatively short period of AlCl 3 treatment in the present study; as findings by Chen et al (2013) in rats fed AlCl 3 for about 6 months showed deposits of amyloid plaques in the hippocampus, perhaps as a result of longer duration of oral exposure to AlCl 3 via the rats' drinking water.…”

Section: Discussionsupporting

confidence: 51%

“…Similarly, intracerebroventricular (ICV) injection of STZ in rodents causes Alzheimer's-like pathology, and this model is one of the choice animal models of AD (Khan et al 2012;Du et al 2014;Khan et al 2015). In addition to ICV STZ, aluminium chloride (AlCl 3 ) administered to rodents either orally or intraperitoneally for several weeks can trigger some AD-like pathology (such as senile plaque, etc) (Chen et al 2013) with variable degrees of neurodegeneration. Nevertheless, neither AlCl 3 nor STZ treatment alone has produced sufficient level of brain lesions in rodent models of diseases of neurodegeneration such as AD; moreover, because of the prevalence of diabetes mellitus among AD subjects (Ott et al 1999), novel animal models of AD disease with diabetes mellitus co-morbidity are desirable.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Characterization of prefrontal cortex microstructure and antioxidant status in a rat model of neurodegeneration induced by aluminium chloride and multiple low-dose streptozotocin

et al. 2015

View full text Add to dashboard Cite

Diabetes mellitus (DM) is a risk factor for Alzheimer's disease (AD), and several individuals with AD are diabetic. Most non-transgenic animal models of AD make use of oral treatment with aluminium chloride (AlCl(3)) to induce brain lesions pathognomonic of the disease. Moreover, streptozotocin (STZ) can induce pathological features of either AD or DM depending on the mode of treatment. In the present study, we characterised prefrontal microanatomy and antioxidant defence system in a rat model of AD confounded by DM, with the objective of assessing the suitability of this model in the study of sporadic AD with DM co-morbidity. Adult Wistar rats were randomly assigned to receive either intraperitoneal STZ (30 mg/kg/day for 3 days; to induce DM), oral AlCl(3) (500 mg/kg/day for 4 weeks; to induce some brain lesions characteristic of AD); or both STZ and AlCl(3) (to induce AD with DM co-morbidity). Untreated rats served as controls. During treatment, blood glucose levels and body weights were evaluated repeatedly in all rats. At euthanasia, prefrontal cortex was homogenized in phosphate buffer solution and the supernatants assayed for some antioxidant enzymes (catalase, CAT; superoxide dismutase, SOD; and reduced glutathione, GSH). Moreover, following perfusion-fixation of the brain, frontal lobes were processed by the haematoxylin and eosin (H&E) or Congo red technique. Our findings showed that in rats co-administered AlCl(3) and STZ (AD + DM rats), prefrontal levels of GSH reduced significantly (p < 0.05), while reductions in SOD and CAT were not significant (p > 0.05) compared with the controls. Moreover, in this model of AD with DM co-morbidity, extensive neuronal cell loss was observed in the prefrontal cortex, but Congophilic deposits were not present. The neurodegenerative lesions and antioxidant deficits characteristic of this AlCl(3) + STZ (AD + DM) rat model were more pronounced than similar lesions associated with mono-treatment with either STZ (DM) or AlCl(3) (AD) alone; and this makes the AlCl(3) + STZ model a suitable option for the study of neurodegenerative diseases (such as AD) with DM co-morbidity.

show abstract

Section: Discussionsupporting

confidence: 51%

Section: Introductionmentioning

confidence: 99%

Characterization of prefrontal cortex microstructure and antioxidant status in a rat model of neurodegeneration induced by aluminium chloride and multiple low-dose streptozotocin

et al. 2015

View full text Add to dashboard Cite

show abstract

“…Implicações no desempenho da memória e aprendizado podem ser observadas em modelos de DA produzidos por alumínio em ratos. Um estudo analisou as consequências das alterações hemodinâmicas, e a associação entre estas e as modificações neuropatológicas na DA induzida por alumínio (Chen et al, 2013). Dois grupos de 10 ratos foram usados no estudo, sendo categorizados como controle, que não receberam a administração do cloreto de alumínio, e o grupo que recebeu a administração do cloreto de alumínio de um a cinco meses.…”

Section: Alumíniounclassified

Substâncias administradas para a indução da Doença de Alzheimer em ratos

Cordeiro

Ticli

Cavallet

2019

RSD

View full text Add to dashboard Cite

ResumoAs estimativas sobre a expansão dos casos da Doença de Alzheimer (DA) no mundo indicam a necessidade de constantes estudos sobre essa patologia ainda sem cura. Os estudos têm investigado a DA em modelos animais não-humanos utilizando substâncias químicas que induzem à DA. O presente estudo teve por objetivo realizar uma revisão da literatura sobre as substâncias usadas em laboratório para reproduzir a DA em ratos. Foram selecionados 44 de 111 estudos analisados, mantendo apenas os artigos que induziram a DA por substâncias químicas. As substâncias identificadas foram o alumínio, a beta-amiloide, a colchicina, a dgalactose, a escopolamina, a estreptozocina e a homocisteína. Verificou-se que dos 44 artigos, a substância mais utilizada foi a beta-amiloide, principal biomarcador da DA. Embora diferentes estudos tenham replicado resultados que simulam a ocorrência de DA em ratos e os tratamentos realizados com ratos em laboratório pareçam promissores, nenhuma cura foi encontrada ainda.Palavras-chave: Doença de Alzheimer; indução; substâncias químicas; ratos; beta-amiloide.Res., Soc. Dev. 2019; 8(6):e486974 AbstractEstimates of the progressive expansion of Alzheimer's disease (AD) worldwide indicate the need for constant studies on this pathology, still without cure. Studies have investigated AD in non-human animal models using substances that induced AD. The present study aimed to review the literature on the substances and procedures used in laboratory to reproduce AD in rats. We selected 44 of 111 studies analyzed, keeping only papers that induced AD by chemical substances. The identified substances were aluminum, beta-amyloid, colchicine, d-galactose, scopolamine, streptozocin and homocysteine. It was verified that of the 44 articles, the most used substance was beta-amyloid, the main biomarker of AD. Although different studies have replicated results that simulate the occurrence of AD in rats and the treatments performed with rats in the laboratory appear promising, no cure has yet been found. ResumenLas estimaciones sobre la expansión de los casos de la enfermedad de Alzheimer (EA) en el mundo indican la necesidad de constantes estudios sobre esta patología aún sin cura. Los estudios han investigado la EA en modelos animales no humanos utilizando sustancias químicas que inducen a la EA. El presente estudio tuvo como objetivo realizar una revisión de la literatura sobre las sustancias usadas en laboratorio para reproducir la EA en ratas. Se seleccionaron 44 de 111 estudios analizados, manteniendo sólo los artículos que indujeron a EA por sustancias químicas. Las sustancias identificadas fueron el aluminio, la beta-amiloide, la colchicina, la d-galactosa, la escopolamina, la estreptozocina y la homocisteína. Se comprobó que de los 44 artículos, la sustancia más utilizada fue la beta-amiloide, principal biomarcador de la EA. Aunque diferentes estudios han replicado resultados que simulan la ocurrencia de EA en ratas y los tratamientos realizados con ratas en laboratorio parecen prometedores, no se ha encontrad...

show abstract

“…Al is not a redox active metal, but it is pro-oxidant and can induce the formation of reactive oxygen species (ROS), causing oxidative stress and cell damage in diverse tissues, including the liver and brain [10, 11]. Some lactic acid bacteria (LAB) strains have been shown to scavenge ROS and possess antioxidative ability, thus providing protection against oxidative stress and lipid peroxidation [12].…”

Section: Introductionmentioning

confidence: 99%

The therapeutic protection of a living and dead Lactobacillus strain against aluminum-induced brain and liver injuries in C57BL/6 mice

Tian

Zhai

et al. 2017

PLoS ONE

View full text Add to dashboard Cite

Our previous study found that Lactobacillus plantarum CCFM639 had the ability to alleviate acute aluminum (Al) toxicity when the strain was introduced simultaneously with Al exposure. This research was designed to elucidate the therapeutic effects of living and dead L. plantarum CCFM639 against chronic Al toxicity and to gain insight into the protection modes of this strain. Animals were assigned into control, Al only, Al + living CCFM639, and Al + dead CCFM639 groups. The Al exposure model was established by drinking water for the first 4 weeks. The strain was given after Al exposure by oral gavage at 109 colony-forming units once per day for 12 weeks. The results show that the Al binding ability of dead CCFM639 was similar to that of living CCFM639 in vitro. The ingestion of living or dead CCFM639 has similar effects on levels of Al and trace element in tissues, but living strains led to more significant amelioration of oxidative stress and improvement of memory deficits in Al-exposed mice. In conclusion, in addition to intestinal Al sequestration, CCFM639 treatment offers direct protection against chronic Al toxicity by alleviation of oxidative stress. Therefore, L. plantarum CCFM639 has a potential as dietary supplement ingredient that provides protection against Al-induced injury.

show abstract

Hemodynamic and Neuropathological Analysis in Rats with Aluminum Trichloride-Induced Alzheimer's Disease

Cited by 22 publications

References 55 publications

Characterization of prefrontal cortex microstructure and antioxidant status in a rat model of neurodegeneration induced by aluminium chloride and multiple low-dose streptozotocin

Characterization of prefrontal cortex microstructure and antioxidant status in a rat model of neurodegeneration induced by aluminium chloride and multiple low-dose streptozotocin

Substâncias administradas para a indução da Doença de Alzheimer em ratos

The therapeutic protection of a living and dead Lactobacillus strain against aluminum-induced brain and liver injuries in C57BL/6 mice

Contact Info

Product

Resources

About