scholarly journals Neurotensin Receptor Involvement in the Rise of Extracellular Glutamate Levels and Apoptotic Nerve Cell Death in Primary Cortical Cultures after Oxygen and Glucose Deprivation

2007 ◽  
Vol 18 (8) ◽  
pp. 1748-1757 ◽  
Author(s):  
T. Antonelli ◽  
M. C. Tomasini ◽  
J. Fournier ◽  
R. Mazza ◽  
S. Tanganelli ◽  
...  
Keyword(s):  
Cell Death ◽  
Nerve Cell ◽  
Glucose Deprivation ◽  
Extracellular Glutamate ◽  
Oxygen And Glucose Deprivation ◽  
Neurotensin Receptor ◽  
Cortical Cultures ◽  
Nerve Cell Death

Predicting Alzheimer's Disease Progression by Combining Multiple Measures

2021 ◽  
Author(s):  
Nour Zawawi ◽  
Heba Gamal Saber ◽  
Mohamed Hashem ◽  
Tarek F.Gharib
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Death ◽  
Early Diagnosis ◽  
Nerve Cell ◽  
Neurological Examination ◽  
Medical Data ◽  
Complex Interactions ◽  
Dementia Patients ◽  
Nerve Cell Death

Alzheimer's disease (AD) is a degenerative brain ailment that affects millions worldwide. It is the most common form of dementia. Patients with an early diagnosis of Alzheimer's disease have a strong chance of preventing additional brain damage by halting nerve cell death. At the same time, it begins to progress several years before any symptoms appear. The variety of data is the biggest problem encountered during diagnosis. Neurological examination, brain imaging, and often asked questions from his connected closed relatives are the three forms of data that a neurologist or geriatrics employs to diagnose patients. One of the biggest questions which need answering is the choice of a convenient feature. The main objective of this paper is to help neurologists or geriatricians diagnose patient conditions. It proposes a new hybrid model for features extracted from medical data. It discusses AD's early diagnosis and progression for all features considered in the diagnosis and their complex interactions. It proves to have the best accuracy when compared with the state-ofthe-art algorithm. Also, it proves to be more accurate against some recent research ideas. It got 95% in all cases, considering this work focused more on increasing the number of instances in comparison.

ATP as a marker of excitotoxin-induced nerve cell death in vivo

1987 ◽  
Vol 70 (3-4) ◽  
pp. 349-356 ◽  
Author(s):  
Annamaria Vezzani ◽  
L. Sangalli ◽  
Hui -Qiu Wu ◽  
R. Schwarcz
Keyword(s):  
Cell Death ◽  
Nerve Cell ◽  
Nerve Cell Death

scholarly journals High-Fat-High-Fructose Diet Decreases Hippocampal Neuron Number in Male Rats

2020 ◽  
Vol 12 (1) ◽  
pp. 1-7
Author(s):  
Inggita Kusumastuty ◽  
Frinny Sembiring ◽  
Sri Andarini ◽  
Dian Handayani
Keyword(s):  
Cell Death ◽  
Nerve Cell ◽  
Hippocampal Neurons ◽  
Sprague Dawley ◽  
High Fat ◽  
Group I ◽  
Sprague Dawley Rats ◽  
High Fructose ◽  
Group Ii ◽  
Nerve Cell Death

BACKGROUND: Consumption of foods and drinks high in energy, fat, and/or sugar beyond the recommended quantities can cause obesity, which triggers the incidence of brain nerve cell death related to oxidative stress, high levels of tumor necrosis factor (TNF)-α and triglycerides, and low high-density lipoprotein (HDL) levels. Progressive nerve cell death causes decreasing cognitive performance. This study aims to prove that an American Institute of Nutrition committee in 1993 (AIN-93M) diet modified with high-fat-high-fructose (HFHF) can decrease the number of hippocampal neurons. A decrease in the number of hippocampal neurons indicates progressive nerve cell death.METHODS: An experimental study using a post-test control group design was carried out using male Sprague Dawley rats. Samples were selected using simple random sampling to divide them into two groups, Group I was AIN-93M-modified HFHF diet (n=14) and Group II was AIN-93M standard (n=16). The number of visible neurons was measured in the hippocampus area of Sprague Dawley rats’ brains, stained with haemotoxylin and eosin (H&E) and scanned under 400x magnification. Neurons were counted in 10 visual fields using the "Cell_Count" application.RESULTS: The data were analysed by Pearson’s correlation test using SPSS. The results show that rats in Group I had a greater weight gain and fewer neurons than those in the Group II (p=0.023, r=-0.413).CONCLUSION: The consumption of foods high in fat and fructose can cause an increase in nerve cell death, as shown by the decrease in the number of hippocampal neurons.KEYWORDS: brain nerve cells, high fat, high fructose, increased body weight

scholarly journals High-density lipoprotein protects cardiomyocytes against necrosis induced by oxygen and glucose deprivation through SR-B1, PI3K, and AKT1 and 2

2018 ◽  
Vol 475 (7) ◽  
pp. 1253-1265 ◽  
Author(s):  
Kristina K. Durham ◽  
Kevin M. Chathely ◽  
Bernardo L. Trigatti
Keyword(s):  
Cell Death ◽  
High Density Lipoprotein ◽  
Ischemia Reperfusion ◽  
Density Lipoprotein ◽  
Glucose Deprivation ◽  
High Density ◽  
Dependent Manner ◽  
Protective Effects ◽  
Oxygen And Glucose Deprivation ◽  
Ventricular Cardiomyocytes

The cardioprotective lipoprotein HDL (high-density lipoprotein) prevents myocardial infarction and cardiomyocyte death due to ischemia/reperfusion injury. The scavenger receptor class B, type 1 (SR-B1) is a high-affinity HDL receptor and has been shown to mediate HDL-dependent lipid transport as well as signaling in a variety of different cell types. The contribution of SR-B1 in cardiomyocytes to the protective effects of HDL on cardiomyocyte survival following ischemia has not yet been studied. Here, we use a model of simulated ischemia (oxygen and glucose deprivation, OGD) to assess the mechanistic involvement of SR-B1, PI3K (phosphatidylinositol-3-kinase), and AKT in HDL-mediated protection of cardiomyocytes from cell death. Neonatal mouse cardiomyocytes and immortalized human ventricular cardiomyocytes, subjected to OGD for 4 h, underwent substantial cell death due to necrosis but not necroptosis or apoptosis. Pretreatment of cells with HDL, but not low-density lipoprotein, protected them against OGD-induced necrosis. HDL-mediated protection was lost in cardiomyocytes from SR-B1−/− mice or when SR-B1 was knocked down in human immortalized ventricular cardiomyocytes. HDL treatment induced the phosphorylation of AKT in cardiomyocytes in an SR-B1-dependent manner. Finally, chemical inhibition of PI3K or AKT or silencing of either AKT1 or AKT2 gene expression abolished HDL-mediated protection against OGD-induced necrosis of cardiomyocytes. These results are the first to identify a role of SR-B1 in mediating the protective effects of HDL against necrosis in cardiomyocytes, and to identify AKT activation downstream of SR-B1 in cardiomyocytes.

scholarly journals The Activation of Dopamine D4 Receptors Inhibits Oxidative Stress-Induced Nerve Cell Death

2001 ◽  
Vol 21 (16) ◽  
pp. 6069-6076 ◽  
Author(s):  
Kumiko Ishige ◽  
Qi Chen ◽  
Yutaka Sagara ◽  
David Schubert
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Nerve Cell ◽  
Nerve Cell Death
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