Brain

Bradley, Alys; Bertrand, Lise; Rao, Deepa B.; Hall, Dianne; Sharma, Alok

doi:10.1016/b978-0-12-391448-4.00013-7

Cited by 4 publications

(3 citation statements)

References 47 publications

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“…Fischer-344 albino rats present spontaneous age-related dystrophy, which targets many tissues such as the cornea, renal tubules, and vascular internal laminae [45,46]. Furthermore, several studies describe retinal age-dependent impairments with a progressive reduction in visual evoked potential amplitude and electroretinographic responses [47] as well as a continuous loss of photoreceptors in the peripheral retina [48] probably due to Müller cell dysfunction [49].…”

Section: Fischer-344 Rats (Fischer)mentioning

confidence: 99%

Retinal Neurodegeneration: Correlation between Nutraceutical Treatment and Animal Model

et al. 2021

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Retinal diseases can be induced by a variety of factors, including gene mutations, environmental stresses and dysmetabolic processes. The result is a progressive deterioration of visual function, which sometimes leads to blindness. Many treatments are under investigation, though results are still mostly unsatisfactory and restricted to specific pathologies, particularly in the case of gene therapy. The majority of treatments have been tested in animal models, but very few have progressed to human clinical trials. A relevant approach is to study the relation between the type of treatments and the degenerative characteristics of the animal model to better understand the effectiveness of each therapy. Here we compare the results obtained from different animal models treated with natural compounds (saffron and naringenin) to anticipate the potentiality of a single treatment in different pathologies.

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Section: Fischer-344 Rats (Fischer)mentioning

confidence: 99%

Retinal Neurodegeneration: Correlation between Nutraceutical Treatment and Animal Model

et al. 2021

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“…Therefore, in this study Nissl stain was used to identify Nissl bodies and extend neuronal damage in the hippocampus CA3 region which contains pyramidal cells. This method can reveal the characteristic morphological alteration of chromatolysis, which is a reactive change occurring in the cell body of damaged neurons, involving the dispersal and redistribution of Nissl bodies (Bradley et al 2018). Another typical morphologi- cal change is dark neurons that occur in many stroke types, such as traumatic brain injury, which may be observed through various staining methods, such as H&E, Nissl, and silver stain (Ooigawa et al 2006).…”

Section: Discussionmentioning

confidence: 99%

Study of neuroprotective activity of new acetylcholinesterase inhibitors TVA and TVS in experimental model of Alzheimer’s disease

Gasparyan¹,

Buloyan²,

Harutyunyan³

et al. 2022

RRP

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Introduction: Alzheimer’s disease (AD) is a severe neurodegenerative disease characterized by loss of synaptic connection between neurons of the cortex and subcortical regions. The cholinergic deficit is a consistent and early finding in AD, hence acetylcholinesterase inhibitors (AChEIs) are used for symptomatic improvement of AD. Most of these therapeutic agents are hepatotoxic, leading to liver failure and other complications. Therefore, the study of new AChEIs with less toxic impact and better effectivity is a topical challenge. In view of this, we synthesized novel chemical compounds: TVA and TVS that possess AChEI activity and studied their neuroprotective effect in an experimental AD model. Materials and methods: Studies were performed on white rats. Acute toxicity studies were performed by Karber’s method. AD was induced via bilateral intracerebroventricular administration of Aβ 25–35. Histopathological examinations were performed in the hippocampus and the entorhinal cortex. Liver tissue was additionally examined to monitor the hepatotoxicity of these compounds. Results: Studies of the hippocampus showed that compared to control and TVA-treated groups, under the influence of TVS there were few morphological alterations. Experimental groups showed an increase in the glial cell count, compared to the intact animals. In comparison to the AD group, the increase in microglia was not that prominent under the action of the novel compounds. Under the influence of TVA and TVS, the entorhinal cortex was more susceptible to neuronal injury, although TVS protected pyramidal neurons. Also, the group treated with TVA had signs of acute liver damage, while under the influence of TVS there were no signs of liver changes. Discussion: Histopathological examination showed that the neurodegenerative processes in the hippocampus, as well as in the entorhinal cortex, were significantly reduced under the influence of TVS, compared with the control group. At the same time, TVA had no significant effect on the protection of neuronal cells. Also, TVS was less toxic, and there was no sign of hepatotoxicity during the experiments. Conclusion: These studies demonstrated that TVS possesses neuroprotective activity and reduces neuronal damage induced by Aβ. Graphical abstract:

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“…The significant positive correlation between ischemic volume and the volume of missing tissue also points in this direction, as unrelated artefacts would not have shown any correlation. Therefore, the remaining Neurotrace+ surrounding tissue can be considered part of the penumbra with regenerating neurons showing a higher Neurotrace signal when compared to the rest of the brain [56] [57] [58] [59]. The evaluation of neuronal survival in the remaining Neurotrace+ tissue using stereology showed no significant differences in cell density between groups.…”

Section: Discussionmentioning

confidence: 99%

A Primeval Mechanism of Tolerance to Desiccation Based on Glycolic Acid Saves Neurons from Ischemia in Mammals by Reducing Intracellular Calcium-Mediated Excitotoxicity

Chovsepian¹,

Berchtold

Winek

et al. 2020

Preprint

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Stroke is the second leading cause of death and disability worldwide. Current treatments, like pharmacological thrombolysis or mechanical thrombectomy, re-open occluded arteries but do not protect against ischemia-induced damage caused before reperfusion or ischemia/reperfusion-induced neuronal damage. It has been shown that knocking out djr-1.1 and djr-1.2 or glod-4 results in a decreased tolerance to anhydrobiosis in C elegans dauer larva and that Glycolic Acid (GA) can rescue this phenotype. During the process of desiccation/rehydration, a metabolic stop/start similar to the one observed during ischemia/reperfusion occurs. In this study we tested the protective effect of GA against ischemia in three different models (oxygen-glucose deprivation in vitro and Global cerebral ischemia as well as Middle Cerebral Artery Occlusion in vivo). Our results show that GA, given during reperfusion, strongly protects against ischemia-induced neuronal death, reduces the mortality in mice with large infarcts, significantly reduces the ischemic area in the brain and improves the functional outcome. The effect of GA is stronger when the substance is applied near the damaged tissue (i.e. directly to the neurons in vitro or intra-arterially via the internal carotid artery in vivo). These results suggest that GA treatment has the potential to dramatically reduce the mortality and disability caused by stroke in patients.

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Brain

Cited by 4 publications

References 47 publications

Retinal Neurodegeneration: Correlation between Nutraceutical Treatment and Animal Model

Retinal Neurodegeneration: Correlation between Nutraceutical Treatment and Animal Model

Study of neuroprotective activity of new acetylcholinesterase inhibitors TVA and TVS in experimental model of Alzheimer’s disease

A Primeval Mechanism of Tolerance to Desiccation Based on Glycolic Acid Saves Neurons from Ischemia in Mammals by Reducing Intracellular Calcium-Mediated Excitotoxicity

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