Modeling Alzheimer's disease with non-transgenic rat models

Lecanu, Laurent; Papadopoulos, Vassilios

doi:10.1186/alzrt171

Cited by 63 publications

(34 citation statements)

References 86 publications

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“…Although the cause of AD remains unclear, Aβ accumulation in the brain was proposed to play a major role in the onset of this disease [35,36]. Partial reproduction of AD neuropathological conditions and cognitive deficits can be achieved with pharmacological drug-induced approaches Evidence-Based Complementary and Alternative Medicine and Aβ overexpression [37]. In this study, Aβ-induced neurotoxicity (AD model) was chosen due to the ability of the Aβ protein-peptide to produce the symptoms and pathophysiology that mimics the slow evolution of AD in humans [19,38].…”

Section: Discussionmentioning

confidence: 99%

Neuroprotection of Tropical Fruit Juice Mixture via the Reduction of iNOS Expression and CRH Level in β‐Amyloid‐Induced Rats Model of Alzheimer’s Disease

Ooi

Munawar

Rosli

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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This study aimed to determine the effects of tropical fruit juice mixture (pomegranate, white guava, and Roselle) on biochemical, behavioral, and histopathological changes of β-amyloid- (Aβ-) induced rats. Formulation 8 (F8) of tropical fruit juice mixture was chosen for this present study due to its high phenolic content and antioxidant capacity. Forty Wistar male rats were divided into five groups: dPBS (sham-operated control), dAβ (Aβ control), JPBS (F8 and PBS), JAβ (F8 and Aβ), and IBFAβ (ibuprofen and Aβ). F8 (5 ml/kg BW), and ibuprofen (10 ml/kg BW) was given orally daily for four weeks before the intracerebroventricular infusion of Aβ for two weeks. Histological analysis and neuronal count of hippocampus tissue in the Cornu Ammonis (CA1) region showed that supplementation with F8 was able to prevent Aβ-induced tissue damage and neuronal shrinkage. However, no significant difference in locomotor activity and novel object recognition (NOR) percentage was detected among different groups at day 7 and day 14 following Aβ infusion. Only effect of time differences (main effect of day) was observed at day 7 as compared to day 14, where reduction in locomotor activity and NOR percentage was observed in all groups, with F (1, 7) = 6.940, p<0.05 and F (1, 7) = 7.152, p<0.05, respectively. Besides, the MDA level of the JAβ group was significantly lower (p<0.01) than that of the dPBS group. However, no significant changes in SOD activity were detected among different groups. Significant reduction in plasma CRH level (p<0.05) and iNOS expression (p<0.01) in the brain was detected in the JAβ group as compared to the dAβ group. Hence, our current findings suggest that the tropical fruit juice mixture (F8) has the potential to protect the rats from Aβ-induced neurotoxicity in brain hippocampus tissue possibly via its antioxidant properties and the suppression of iNOS expression and CRH production.

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Section: Discussionmentioning

confidence: 99%

Neuroprotection of Tropical Fruit Juice Mixture via the Reduction of iNOS Expression and CRH Level in β‐Amyloid‐Induced Rats Model of Alzheimer’s Disease

Ooi

Munawar

Rosli

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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“…Chronic D-gal administration produces cognitive dysfunction and neurodegeneration similar to that in aged rats and thus has a well proved AD rat model [4]. Moreover, AD was characterized histopathologically by formation of Aβ plaques in the brain tissue and intracerebroventricular administration of Aβ in rats produces AD or dementia [12]. Thus, in the present investigation SD was induced by chronic administration of D-gal and Aβ1-42 in a rat model.…”

Section: Discussionmentioning

confidence: 72%

Cepharanthine promotes the effect of dexmedetomidine on the deposition of β-amyloid in the old age of the senile dementia rat model by regulating inflammasome expression

Wu¹,

Cao²,

Wang³

et al. 2019

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Aim of the study: The present study evaluates the synergistic effect of cepharanthine (CP) with dexmedetomidine (DEM) on the deposition of β-amyloid (Aβ) in the brain tissue of senile dementia (SD) rats. Material and methods: Senile dementia was induced by injecting D-gal intraperitoneally 60 mg/kg/day for six weeks and Aβ1-42 (5 µl) intracranially. The effect of cepharanthine and dexmedetomidine was estimated by determining the cognitive function and neurological function score. Moreover, mediators of inflammation, parameters of oxidative stress and reactive oxygen species (ROS) were determined in the brain tissue of senile dementia rats. Mitochondrial membrane permeability and deposition of Aβ1-42 was estimated in senile dementia rats. Western blot assay and reverse transcription polymerase chain reaction (RT-PCR) was performed for the expression of proteins and genes in the brain tissue of senile dementia rats. Results: Data of the study reveal that cepharanthine alone and in combination with dexmedetomidine improves the neurological function score and cognitive function in SD rats. Moreover, parameters of oxidative stress, inflammatory mediators and production of ROS in CP, DEM and CP + DEM treated groups were compared to the SD group of rats. Treatment with CP, DEM and CP + DEM ameliorates the altered expression of NLRP3 pathway and deposition of Aβ in the brain tissue of SD rats. Conclusions: In conclusion, data reveal that cepharanthine ameliorates the deposition of Aβ and NLRP3 pathway in SD rats. Moreover, cepharanthine treatment with dexmedetomidine shows the synergistic effect against the aged SD rat model.

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“…It should not be too surprising that some investigators have termed Alzheimer's disease as diabetes 3 because of its similarity to diabetes [9]. Many investigators have switched to this STZ -ALZ based superior standard mouse model to study possible inhibitors of the disease Kimura and Lecanu and Papadopoulous [13,14].…”

Section: Streptozotocin Generates Peroxynitrite Luminescence Which Rementioning

confidence: 99%

Streptozotocin Generates Peroxynitrite Luminescence Which Reveals the Cause of Diabetes 1,2 and 3 (Alzheimer’s disease)

Dyke¹,

Geldenhuys²,

Robart³

2017

IJOAO

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The fundamental basis of diabetes continues to go unrecognized and untreated. Depending on the type of diabetes i.e; 1 or 2, treatment consists of insulin injections (1) or antidiabetic drugs that lower blood glucose and hopefully hemoglobin A1C as well (2) Often patients with type 2 are asked to lose weight, exercise more vigorously as well and more frequently. Previously, using a diabetic-streptozotocin (STZ) rat model, we demonstrated that diabetes and cataracts could be entirely prevented using equimolar amounts of STZ and a nitric oxide oxidizing compound called sodium carboxy-PTIO. This indicated that STZ generated a nitric oxide-oxygen based toxin that could be destroyed in vivo. The treatment completely prevented STZ from increasing blood glucose and all the signs of diabetes-including cataracts were prevented. Later work indicated how the STZ-diabetes pathway was likely created. Now, we demonstrate that STZ actually generates the oxidizing and nitrating peroxide known as peroxynitrite (OONO-). In the cases of diabetes 1,2 most or all of many anti-diabetic drugs only control the level of blood glucose, and many with considerable side effects. We demonstrate in diabetic children over a three year period that even with tight dietary control of blood glucose, diabetes still persists. This diabetic damage stems from peroxynitrite. Using STZ to generate peroxynitrite in animals, we demonstrate that a variety of nitration targets can diminish peroxynitite which is the most important step in controlling both diabetes and possibly Alzheimer's disease since recent data links diabetes and Alzheimer's disease.

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Modeling Alzheimer's disease with non-transgenic rat models

Cited by 63 publications

References 86 publications

Neuroprotection of Tropical Fruit Juice Mixture via the Reduction of iNOS Expression and CRH Level in β‐Amyloid‐Induced Rats Model of Alzheimer’s Disease

Neuroprotection of Tropical Fruit Juice Mixture via the Reduction of iNOS Expression and CRH Level in β‐Amyloid‐Induced Rats Model of Alzheimer’s Disease

Cepharanthine promotes the effect of dexmedetomidine on the deposition of β-amyloid in the old age of the senile dementia rat model by regulating inflammasome expression

Streptozotocin Generates Peroxynitrite Luminescence Which Reveals the Cause of Diabetes 1,2 and 3 (Alzheimer’s disease)

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