Understanding the Therapeutic Approaches for Neuroprotection
Nazrana PayalLalit SharmaAditi SharmaYahya Hosan HobaniiMashael HakamiNemat AliSummya RashidMonika SachdevaMonica GulatiShivam YadavSridevi ChigurupatiAbhiav SinghHaroon KhanTapan Behl
4
Citation
161
Reference
10
Related Paper
Citation Trend
Abstract:
Abstract: The term “neurodegenerative disorders” refers to a group of illnesses in which deterioration of nerve structure and function is a prominent feature. Cognitive capacities such as memory and decision-making deteriorate as a result of neuronal damage. The primary difficulty that remains is safeguarding neurons since they do not proliferate or regenerate spontaneously and are therefore not substituted by the body after they have been damaged. Millions of individuals throughout the world suffer from neurodegenerative diseases. Various pathways lead to neurodegeneration, including endoplasmic reticulum stress, calcium ion overload, mitochondrial dysfunction, reactive oxygen species generation, and apoptosis. Although different treatments and therapies are available for neuroprotection after a brain injury or damage, the obstacles are inextricably connected. Several studies have revealed the pathogenic effects of hypothermia, different breathed gases, stem cell treatments, mitochondrial transplantation, multi-pharmacological therapy, and other therapies that have improved neurological recovery and survival outcomes after brain damage. The present review highlights the use of therapeutic approaches that can be targeted to develop and understand significant therapies for treating neurodegenerative diseases.Privation
Cite
Citations (8)
Cite
Citations (311)
Background: Environmental toxins, nutritional discrepancies, genetic predispositions, and lifestyle modifications induce a variety of stresses on the human brain and body. Such chronic stressors can influence the onset and progression of neurodegeneration via cellular alterations. In this systematic review, we have discussed the role of oxidative stress in causing neurodegeneration. Moreover, the chemical, metallic and other etiological factors that stimulate oxidative stress and results in the development of neurodegenerative disorders are also explored and summarized.
Methodology: A systematic review was conducted to investigate the impact of oxidative stress on the human brain in relation to neurodegeneration. The human studies focusing on neurobiology and cellular changes in brain, investigating the pathway of oxidative stress leading to neurodegeneration through mitochondrial dysfunction and cellular alterations, published during 1st January 2000 to 31st March 2019 were identified and included in this systematic review.
Result: Following the PRISMA guidelines, 13 out of 1169 studies met the eligibility criteria and were included in the quantitative synthesis and screening. These studies focused on the features like cellular factors, metal exposure, and aging, inducing oxidative stress-related neurodegeneration. 6 studies described mitochondrial alterations resulting in oxidative stress due to an increase in the production of reactive oxygen species (ROS), oxidation of proteins, peroxidation of lipid and damages to the deoxyribonucleic acid (DNA) and ribonucleic acid (RNA). While the data from 5 studies suggested the loss of mitochondrial activity in response to metal exposure. 2 experimental studies specified the effect of aging and self-implication of oxidative stress in the brain.
Conclusion: Although there are sufficient evidence that supported the hypothesis that stress is significantly associated with neurodegeneration but it is still not considered as a primary instigator in neurodegenerative disorders. However, it can be concluded on the basis of this review that it has been involved in the propagation of cellular alterations and mitochondrial dysfunction that further leads to neurodegeneration.
Cite
Citations (1)
Brain and spinal cord (CNS) trauma typically kill a number of neurons, but even more neurons are killed by secondary causes triggered by the initial trauma. Thus, a minor insult may rapidly cause the death of a vastly larger number of neurons and complete paralysis. The best mechanism for reducing the extent of neurological deficits is to minimize the number of neurons killed by post‐trauma sequelae. Neuroprotection techniques take many diverse forms with a breadth too great for a short review. Therefore, this review focuses on the neuroprotection provided by hypothermia and a number of other neuroprotective techniques, when administered singly or in combination, because it is generally found that combinations of applications lead to significantly better neuroprotection than is achieved by any one alone. The combinatorial approach to neuroprotection holds great promise for enhancing the degree of neuroprotection following trauma, leading to maximum maintenance of neurological function.
Cite
Citations (9)
Chronic neurodegenerative diseases, such as prion diseases or Alzheimer's disease, are associated with progressive accumulation of host proteins which misfold and aggregate. Neurodegeneration is restricted to specific neuronal populations which show clear accumulation of misfolded proteins, whilst neighbouring neurons remain unaffected. Such data raise interesting questions about the vulnerability of specific neuronal populations to neurodegeneration and much research has concentrated only on the mechanisms of neurodegeneration in afflicted neuronal populations. An alternative, undervalued and almost completely unstudied question however is how and why neuronal populations are resilient to neurodegeneration. One potential answer is unaffected regions do not accumulate misfolded proteins, thus mechanisms of neurodegeneration do not become activated. In this perspectives, we discuss novel data from our laboratories which demonstrate that misfolded proteins do accumulate in regions of the brain which do not show evidence of neurodegeneration and further evidence that microglial responses may define the severity of neurodegeneration.
Cite
Citations (3)
Neuronal cells are extremely vulnerable and have a limited capacity for self-repair in response to injury. For those reasons, there is obvious interest in limiting neuronal damage. Mechanisms and strategies used in order to protect against neuronal injury, apoptosis, dysfunction, and degeneration in the central nervous system are recognized as neuroprotection. Neuroprotection could be achieved through several classes of natural and synthetic neuroprotective agents. However, considering the side effects of synthetic neuroprotective agents, the search for natural neuroprotective agents has received great attention. Recently, an increasing number of studies have identified neuroprotective properties of chitosan and its derivatives; however, there are some significant challenges that must be overcome for the success of this approach. Hence, the objective of this review is to discuss neuroprotective properties of chitosan and its derivatives.
Cite
Citations (152)
It has been demonstrated that oxidative stress has a ubiquitous role in neurodegenerative diseases. Major source of oxidative stress due to reactive oxygen species (ROS) is related to mitochondria as an endogenous source. Although there is ample evidence from tissues of patients with neurodegenerative disorders of morphological, biochemical, and molecular abnormalities in mitochondria, it is still not very clear whether the oxidative stress itself contributes to the onset of neurodegeneration or it is part of the neurodegenerative process as secondary manifestation. This paper begins with an overview of how oxidative stress occurs, discussing various oxidants and antioxidants, and role of oxidative stress in diseases in general. It highlights the role of oxidative stress in neurodegenerative diseases like Alzheimer's, Parkinson's, and Huntington's diseases and amyotrophic lateral sclerosis. The last part of the paper describes the role of oxidative stress causing deregulation of cyclin-dependent kinase 5 (Cdk5) hyperactivity associated with neurodegeneration.
Cite
Citations (282)
Herbal bioactive compounds have been investigated to possess neuroprotective properties. They are involved in the modulation of different signaling pathways that may facilitate neuroprotection. In this brief review, some of the promising compounds and their potential neuroprotective effects have been reported. They can be potential sources of therapeutics for neurodegenerative disorders.
KEYWORDS: neuroprotective, herbal, bioactive compounds, neurodegenerative diseases
Cite
Citations (0)
AMA Pluta R, Bogucka-Kocka A, Ułamek-Kozioł M, et al. Review paperNeurogenesis and neuroprotection in postischemic brain neurodegeneration with Alzheimer phenotype: is there a role for curcumin?. Folia Neuropathologica. 2015;53(2):89-99. doi:10.5114/fn.2015.52405. APA Pluta, R., Bogucka-Kocka, A., Ułamek-Kozioł, M., Furmaga-Jabłońska, W., Januszewski, S., & Brzozowska, J. et al. (2015). Review paperNeurogenesis and neuroprotection in postischemic brain neurodegeneration with Alzheimer phenotype: is there a role for curcumin?. Folia Neuropathologica, 53(2), 89-99. https://doi.org/10.5114/fn.2015.52405 Chicago Pluta, Ryszard, Anna Bogucka-Kocka, Marzena Ułamek-Kozioł, Wanda Furmaga-Jabłońska, Sławomir Januszewski, Judyta Brzozowska, and Mirosław Jabłoński et al. 2015. "Review paperNeurogenesis and neuroprotection in postischemic brain neurodegeneration with Alzheimer phenotype: is there a role for curcumin?". Folia Neuropathologica 53 (2): 89-99. doi:10.5114/fn.2015.52405. Harvard Pluta, R., Bogucka-Kocka, A., Ułamek-Kozioł, M., Furmaga-Jabłońska, W., Januszewski, S., Brzozowska, J., Jabłoński, M., and Kocki, J. (2015). Review paperNeurogenesis and neuroprotection in postischemic brain neurodegeneration with Alzheimer phenotype: is there a role for curcumin?. Folia Neuropathologica, 53(2), pp.89-99. https://doi.org/10.5114/fn.2015.52405 MLA Pluta, Ryszard et al. "Review paperNeurogenesis and neuroprotection in postischemic brain neurodegeneration with Alzheimer phenotype: is there a role for curcumin?." Folia Neuropathologica, vol. 53, no. 2, 2015, pp. 89-99. doi:10.5114/fn.2015.52405. Vancouver Pluta R, Bogucka-Kocka A, Ułamek-Kozioł M, Furmaga-Jabłońska W, Januszewski S, Brzozowska J et al. Review paperNeurogenesis and neuroprotection in postischemic brain neurodegeneration with Alzheimer phenotype: is there a role for curcumin?. Folia Neuropathologica. 2015;53(2):89-99. doi:10.5114/fn.2015.52405.
Cite
Citations (32)