Aggregates Modulate Neuronal Survival †Free Samples to Students

Question: Discuss about the Aggregates Modulate Neuronal Survival. Answer: Introduction: The Chosen paper is about neurodegenerative disease, which is caused due to Degeneration or regular date of neuron a cells. Cerium oxide nanoparticle (CeONPs) is believed to be one of the essential element that can be used for the treatment of neurodegenerative disorder. The current paper discusses about importance of Cerium oxide nanoparticle that are used for the treatment of neurological disorder including Alzheimer's and Parkinson's disease. Multiple sclerosis, ischemic stroke and amyotrophic lateral sclerosis are few of the other common forms of Neurological disorders that are discussed in the given paper management. This is one of the main findings of the papers is related to the therapeutic use of the Cerium oxide nanoparticles that seems to have Antioxidant activity within the neurogenetics cells. One of the major cause of Alzheimer's disease is degeneration of brain-derived neurotrophic factor protein (BDNF), which is considered to be the main biomolecules for memory formation inside brain (Castrn and Kojima 2017). The reduced amount of bdnf in brain is directly linked with degradation of neuron cells. The experiment conducted by Cimini et al. (2012) have discussed about the Neuroblastoma cells, which are used in the treatment of Alpha Beta cell line. The CeONPs are used in the purpose of Signal transduction pathway in regeneration of neural cells that are used in memory storage. Alpha beta factor of CeONPs help to induce mitochondrial fragmentation that are used to revive the cells in memory generation management. The use of CeONPs has been effective in the treatment of Parkinson's disease, which is mainly caused due to exposure of neuron cells to manganese. The antioxidant nature of CeONPs used in the measurement of cell metabolism, which is believed to have a significant impact on the regeneration of neural cells. The paper has also discussed about application of CeONPs in treatment of other neurodegenerative disorder including multiple cirrhosis. In vitro experiment has proved that CeONPs can be stabilized with the use of citrate and polyethylene glycol. The future relevant research work needs to accurately focus of on the usages of CeONPs with specific focus on its ROS-scavenging property. It is also important to design drugs for better encapsulating potential of CeONPs. This will help in the purpose of Oxidative stress reduction and thereby help in the purpose of fibrillation and kintices of CNS protein. All the family of protein under CNS need to be given special focus in order to improve the treatment quality of both Alzheimer's and Parkinson's disease. Contribution of the paper in the study of neurodegenerative disease The main focus point about the selected research paper is the discussion made related to CeONPs and its oxidative property that are used in the treatment of neurodegenerative diseases. Previous research experiment by Dillon et al. (2011), have describe the importance of Cerium Oxide Nanoparticles to protect against the MPTP induced Dopaminergic Neurodegeneration. The mouse model has been used for the given purpose the understand the impact of the same on Parkinson's disease. The free radicals of CeONPs that act as the free scavenger has been studied to understand its impact in the purpose of regeneration. This previous research work has helped the current paper to review the same in context of future potential of CeONPs as nanoparticles that are used for the purpose of Neurodegenerative treatment. The research work by DeCoteau et al. (2016), have describe the function of CeONPs that are used to neutralize reactive Oxygen and nitrogen species, which is believed to induce oxidative stress. This is responsible for causing amyotrophic lateral sclerosis that is one of the major Neurodegenerative diseases. The current paper has therefore been able to review the antioxidant property of cerium oxide nanoparticle. Potential advancement in the neural and clinical settings The potential advancement that is being highlighted in the paper is the advancement in the treatment of the neurodegerative disease. According to Naz et al. (2017), CeONP can be effectively used in the treatment of Alzheimers disease. The treatment of CeONP is mainly based on the anti-xidant activity of CeONP. This is stated as the potential advancement because, according to Padurariu et al. (2013), one of the leading biological mechanism behind the development of the Alzheimers disease is the increase in the level of the oxidative stress as highlighted by the stress theory of agving. Thus this antoxidnat therapy mainly targets the reactive oxygen species which is generated from the biochemical mechains of ageining and thereby helping in the treatement of Alzheimers disease. Earlier the main treatment of the Alzheimers diease mainly involved around the use of transcranial brain stimulation but according to Nardone et al. (2012) transcranial brain stimulation induce short-duration ben eficial effects. Thus were not optimally capbale towards establishing significant evidence for therapeutic efficacy. According to Douaud et al. (2013), Vitaim B is also use towards the treatment of the alzheimers diease but this therapy is mostly directed towards the gray matter atrophy and thus in majority of times is regarded to be non-specific. The results highlighted in the study of Naz et al. (2017) showed that the CeONP is effective in the disruption of the neurofibrirally tangles which are deposited in the hippocampus of the brain. Thus the target of CeONP is specific and thereby making it a potential therapy plan of in the domain of the dieases related to neuroscience. Accoridng to Naz et al. (2017), antioxidants property of CeONP can also be utilised for the treatment of the another neurodegerative disease, Parkinson, multiple sclerosis, and laterial sceloris. This findings are extremely significant because, this kind of neurdegerative disease is fatal. It mainly effect tha t dopaminergic cells of the brain which increases the level of stress among the neuronal cells via creating disruption in the autophagic catabolism, endiplasmic reticulum stress mitochondrial dysnfunction and loss of calcium homeostatsis. All these biochemical mechanism are extremely significant of miantainng equilibirum in the body and any disruption in this mechanism leads to fatal outcomes (Michel, Hirsch and Hunot 2016). Thus providing a substitute treatment plan in order to treat fatal neurodegerative disease is indeed a significant approach in neurosicnece. Moreover, CeONP provides oxidative stress relief which helps in the possible clearance of the stress factor over the endoplasmic reticulum and over the mitochondria and thereby helping to reduce the chrinicty of the disease (Michel, Hirsch and Hunot 2016). Naz et al. (2017) have further recommended that the presence of amalgamated valence states along with extraordinary antioxidant properties conatined in the CeONPs make th em one of the prospective therapeutic target for the treatment of some of the fatal yet common neurodegerative diseases. The unique redox property possessed by cerium oxide present them as one of the potent antioxidants in comparison to other ROS modulators. Moreover, CeONP have long half life further making them potent for the targeted delivery into the body without loss in the efficiay of the particile. Legal and ethical issues related to the paper There are no significant legal and ethical isssues that can be highlighted in this paper. This because. The paper is mostly based on the summary of the recent findings in the domain of CeONP treatment in variour neurological dieases like Alzheimers diease, Parkinsons diease, multiple sclerosis and lateral scelrosis. However, according to the Paraho et al. (2014), while conducting the systematic review, proper citation of the each are very paper along with thorugh documentation is mandatory in order to avoid the ethical and legal threat of plagiarism. The study conducted by Naz et al. (2017) have succinately referenced all the required citation along with the detailed elaboration in the reference list. However, there are no significant indication of whether the paper selected for the systetamic review is based on the human trials or animal trial. Further elaboration of the trail nature of the paper selected for the review is mandatory in order to make the paper more ethically and lega lly authentic (Parahoo 2014). Reference Castrn, E. and Kojima, M., 2017. Brain-derived neurotrophic factor in mood disorders and antidepressant treatments. Neurobiology of disease, 97, pp.119-126. Cimini, A., DAngelo, B., Das, S., Gentile, R., Benedetti, E., Singh, V., Monaco, A.M., Santucci, S. and Seal, S., 2012. Antibody-conjugated PEGylated cerium oxide nanoparticles for specific targeting of A aggregates modulate neuronal survival pathways. Acta biomaterialia, 8(6), pp.2056-2067. DeCoteau, W., Heckman, K.L., Estevez, A.Y., Reed, K.J., Costanzo, W., Sandford, D., Studlack, P., Clauss, J., Nichols, E., Lipps, J. and Parker, M., 2016. Cerium oxide nanoparticles with antioxidant properties ameliorate strength and prolong life in mouse model of amyotrophic lateral sclerosis. Nanomedicine: Nanotechnology, Biology and Medicine, 12(8), pp.2311-2320. Dillon, C.D., Billings, M., Hockey, K.S., DeLaGarza, L. and Rzigalinski, B.A., 2011. Cerium oxide nanoparticles protect against MPTP-induced dopaminergic neurodegeneration in a mouse model for Parkinsons disease. Nanotechnology, 3, pp.451-454. Douaud, G., Refsum, H., de Jager, C.A., Jacoby, R., Nichols, T.E., Smith, S.M. and Smith, A.D., 2013. Preventing Alzheimers disease-related gray matter atrophy by B-vitamin treatment.Proceedings of the National Academy of Sciences,110(23), pp.9523-9528. Michel, P.P., Hirsch, E.C. and Hunot, S., 2016. Understanding dopaminergic cell death pathways in Parkinson disease.Neuron,90(4), pp.675-691. Nardone, R., Bergmann, J., Christova, M., Caleri, F., Tezzon, F., Ladurner, G., Trinka, E. and Golaszewski, S., 2012. Effect of transcranial brain stimulation for the treatment of Alzheimer disease: a review.International Journal of Alzheimers Disease,2012. Naz, S., Beach, J., Heckert, B., Tummala, T., Pashchenko, O., Banerjee, T. and Santra, S., 2017. Cerium oxide nanoparticles: a radicalapproach to neurodegenerative disease treatment.Nanomedicine,12(5), pp.545-553. Padurariu, M., Ciobica, A., Lefter, R., Lacramioara Serban, I., Stefanescu, C. and Chirita, R., 2013. The oxidative stress hypothesis in Alzheimers disease.Psychiatria Danubina,25(4), pp.0-409. Parahoo, K., 2014.Nursing research: principles, process and issues. Palgrave Macmillan.