scholarly journals Neuroprotection by Micronutrients and Cannabidiol (CBD) in Neurodegenerative Diseases

2020 ◽  
pp. 1-10
Author(s):  
Kedar N. Prasad ◽  
Kedar N. Prasad
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Neurodegenerative Diseases ◽  
Glutamate Receptors ◽  
Clinical Studies ◽  
Cannabinoid Receptors ◽  
Neurological Diseases ◽  
Endocannabinoid System ◽  
Protective Proteins

The major objectives of this review are to elucidate the role of antioxidants and cannabidiol (CBD) in reducing oxidative stress, inflammation, and glutamate levels, which contribute to the pathogenesis of human neurological diseases. Antioxidants act by: (a) donation of electrons to molecules with unpaired electrons to neutralize them, (b) activation of ROS-resistant Nrf2 to enhance the levels of antioxidant enzymes, (c) restoration of deficiency of antioxidants to normal levels, (d) alterations in the expression of microRNAs, which guide their respective mRNAs to translate protective proteins, and (e) prevention of the release and toxicity of glutamate. CBD acts by: (a) activating endocannabinoid system, which consists of anandamide and archidonoylglycerol, cannabinoid receptors CB1R and CB2R, and their synthesizing and degrading enzymes, (b) acting as an agonist to non-cannabinoid receptors, such as dopamine, serotonin, and adenosine, (c) acting as an inhibitor of serotonin re-uptake, and (d) acting as an antagonist to glutamate receptors. Since antioxidants and CBD act primarily by different mechanisms, it is proposed that combination of the two may be more effective than either individually. No review on this topic has been published. Pre-clinical and clinical studies are suggested to test the efficacy of proposed combination in selected neurodegenerative diseases.

scholarly journals Isoprostanes and Neuroprostanes as Biomarkers of Oxidative Stress in Neurodegenerative Diseases

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Elżbieta Miller ◽  
Agnieszka Morel ◽  
Luciano Saso ◽  
Joanna Saluk
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Diseases ◽  
Neurological Diseases ◽  
The Body ◽  
Jakob Disease ◽  
Novel Biomarkers ◽  
The Relationship ◽  
Biomarkers Of Oxidative Stress

Accumulating data shows that oxidative stress plays a crucial role in neurodegenerative disorders. The literature data indicate thatin vivoor postmortem cerebrospinal fluid and brain tissue levels of F2-isoprostanes (F2-IsoPs) especially F4-neuroprotanes (F4-NPs) are significantly increased in some neurodegenerative diseases: multiple sclerosis, Alzheimer's disease, Huntington's disease, and Creutzfeldt-Jakob disease. Central nervous system is the most metabolically active organ of the body characterized by high requirement for oxygen and relatively low antioxidative activity, what makes neurons and glia highly susceptible to destruction by reactive oxygen/nitrogen species and neurodegeneration. The discovery of F2-IsoPs and F4-NPs as markers of lipid peroxidation caused by the free radicals has opened up new areas of investigation regarding the role of oxidative stress in the pathogenesis of human neurodegenerative diseases. This review focuses on the relationship between F2-IsoPs and F4-NPs as biomarkers of oxidative stress and neurodegenerative diseases. We summarize the knowledge of these novel biomarkers of oxidative stress and the advantages of monitoring their formation to better define the involvement of oxidative stress in neurological diseases.

scholarly journals Mathematical and computational modeling of the role of homocysteine in the oxidative process and its influence in neuronal degenerative diseases

2021 ◽  
Vol 42 (1) ◽  
pp. 75
Author(s):  
Ana Gabriela da Silva Freitas ◽  
Gizelle Kupac Vianna ◽  
Claudia Mazza Dias
Keyword(s):  
Oxidative Stress ◽  
Computational Modeling ◽  
Neurodegenerative Diseases ◽  
Neuronal Death ◽  
Computational Models ◽  
Neurological Diseases ◽  
Degenerative Diseases ◽  
Oxidative Process ◽  
Mathematical And Computational Modeling

Degenerative neurological diseases, although common in the population, are difficult to diagnose. However, it is known that most of them are directly related to the so-called oxidative stress. Understanding and evaluating how this process takes place is of great interest and, in this sense, this work extends the existing mathematical and computational models for the oxidative stress process (REIS, 2005; REIS et al., 2006; VIANNA, 2005; VIANNA; REIS; CARVALHO, 2012), incorporating an aspect not previously evaluated, the influence of homocysteine indices on the oxidants present in this process. The results indicate that hyperhomocysteinemia can in fact cause oxidative stress and consequent neuronal death, leading to the appearance of neurodegenerative diseases.

Biobanking for Neurodegenerative Diseases: Challenge for Translational Research and Data Privacy

2021 ◽  
pp. 107385842110366
Author(s):  
Emilia Giannella ◽  
Valentino Notarangelo ◽  
Caterina Motta ◽  
Giulia Sancesario
Keyword(s):  
Neurodegenerative Diseases ◽  
Translational Research ◽  
Data Protection ◽  
Biological Samples ◽  
Data Privacy ◽  
Neurological Diseases ◽  
Great Effort ◽  
General Data Protection Regulation ◽  
In Silico Studies

Biobanking has emerged as a strategic challenge to promote knowledge on neurological diseases, by the application of translational research. Due to the inaccessibility of the central nervous system, the advent of biobanks, as structure collecting biospecimens and associated data, are essential to turn experimental results into clinical practice. Findings from basic research, omics sciences, and in silico studies, definitely require validation in clinically well-defined cohorts of patients, even more valuable when longitudinal, or including preclinical and asymptomatic individuals. Finally, collecting biological samples requires a great effort to guarantee respect for transparency and protection of sensitive data of patients and donors. Since the European General Data Protection Regulation 2016/679 has been approved, concerns about the use of data in biomedical research have emerged. In this narrative review, we focus on the essential role of biobanking for translational research on neurodegenerative diseases. Moreover, we address considerations for biological samples and data collection, the importance of standardization in the preanalytical phase, data protection (ethical and legal) and the role of donors in improving research in this field.

scholarly journals From the Clinic to the Laboratory, and Back Again: Investigations on Cannabinoids and Endocannabinoid System Modulators for Treating Schizophrenia

2021 ◽  
Vol 12 ◽  
Author(s):  
Kurt Leroy Hoffman
Keyword(s):  
Animal Models ◽  
Outcome Measures ◽  
Clinical Studies ◽  
Cannabinoid Receptors ◽  
Endocannabinoid System ◽  
Clinical Work ◽  
Clinical Results ◽  
Cognitive Outcome ◽  
Experimental Drugs ◽  
First Results

The present mini-review focuses on animal models of schizophrenia that have explored the effects of cannabidiol (CBD; a non-psychoactive component of cannabis) or the pharmacological manipulation of the endocannabinoid system on behavioral and cognitive outcome measures. First, results of some relevant clinical studies in this area are summarized, and then pre-clinical work on animal models of schizophrenia based on NMDA receptor antagonism or neurodevelopmental manipulations are discussed. A brief overview is given of the theoretical framework on which these models are based, along with a concise summary of results that have been obtained. Clinical results using CBD for schizophrenia seem promising and its effects in animal models of schizophrenia support its potential as a useful pharmacotherapy. Animal models have been paramount for elucidating the actions of CBD and the function of the endocannabinoid system and for identifying novel pharmacological targets, such as cannabinoid receptors and anandamide. However, more attention needs to be placed on defining and applying independent variables and outcome measures that are comparable between pre-clinical and clinical studies. The objective of this review is, on the one hand, to emphasize the potential of such models to predict clinical response to experimental drugs, and on the other hand, to highlight areas in which research on such models could be improved.

scholarly journals The protective role of CsNPs and CurNPs against DNA damage, oxidative stress, and histopathological and immunohistochemical alterations induced by hydroxyapatite nanoparticles in male rat kidney

2019 ◽  
Vol 8 (5) ◽  
pp. 741-753 ◽  
Author(s):  
Israa F. Mosa ◽  
Mokhtar I. Yousef ◽  
Maher Kamel ◽  
Osama F. Mosa ◽  
Yasser Helmy
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Biological Effects ◽  
Male Rats ◽  
Nuclear Antigen ◽  
Male Rat ◽  
Control Group ◽  
Renal Tubules ◽  
Hydroxyapatite Nanoparticles

Abstract Hydroxyapatite nanoparticles (HAP-NPs) are an inorganic component of natural bone and are mainly used in the tissue engineering field due to their bioactivity, osteoconductivity, biocompatibility, non-inflammatory, and non-toxicity properties. However, the current toxicity data for HAP-NPs regarding human health are limited, and only a few results from basic studies have been published. Therefore, the present study was designed to investigate the beneficial role of chitosan nanoparticles (CsNPs) and curcumin nanoparticles (CurNPs) in alleviating nephrotoxicity induced by HAP-NPs in male rats. The results showed that HAP-NPs caused a reduction in antioxidant enzymes and induced lipid peroxidation, nitric oxide production and DNA oxidation. Moreover, HAP-NP administration was associated with intense histologic changes in kidney architecture and immunoreactivity to proliferating cell nuclear antigen (PCNA). However, the presence of CsNPs and/or CurNPs along with HAP-NPs reduced the levels of oxidative stress through improving the activities of antioxidant enzymes. Also, the rats administered the nanoparticles showed a moderate improvement in glomerular damage which matched that of the control group and showed mild positive reactions to PCNA–ir in glomeruli and renal tubules in the cortical and medullary portions. These novel insights confirm that the presence of chitosan and curcumin in nanoforms has powerful biological effects with enhanced bioactivity and bioavailability phenomena compared to their microphase counterparts. Also, they were able to ameliorate the nephrotoxicity induced by HAP-NPs.

Role of oxidative stress and thiol antioxidant enzymes in nickel toxicity and resistance in strains of the green alga Scenedesmus acutus f. alternans

2001 ◽  
Vol 47 (11) ◽  
pp. 987-993 ◽  
Author(s):  
Varinder K. Randhawa ◽  
Fengzhen Zhou ◽  
Xiaolei Jin ◽  
Czesia Nalewajko ◽  
Donn J. Kushner
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Green Alga ◽  
Nickel Toxicity ◽  
Scenedesmus Acutus ◽  
Thiol Antioxidant

scholarly journals 3,3′-Diindolylmethane Promotes BDNF and Antioxidant Enzyme Formation via TrkB/Akt Pathway Activation for Neuroprotection against Oxidative Stress-Induced Apoptosis in Hippocampal Neuronal Cells

Antioxidants ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 3 ◽  
Author(s):  
Bo Dam Lee ◽  
Jae-Myung Yoo ◽  
Seong Yeon Baek ◽  
Fu Yi Li ◽  
Dai-Eun Sok ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Neurodegenerative Diseases ◽  
Antioxidant Enzyme ◽  
Neuronal Cells ◽  
Akt Pathway ◽  
Heme Oxygenase 1 ◽  
Enzyme Formation ◽  
Induced Apoptosis

3,3′-Diindolylmethane (DIM), a metabolite of indole-3-carbinol present in Brassicaceae vegetables, possesses various health-promoting effects. Nonetheless, the effect of DIM on neurodegenerative diseases has not been elucidated clearly. In this study, we hypothesized DIM may protect neuronal cells against oxidative stress-induced apoptosis by promoting the formation of brain-derived neurotrophic factor (BDNF) and antioxidant enzymes through stabilizing the activation of the tropomyosin-related kinase receptor B (TrkB) cascade and we investigated the effect of DIM on oxidative stress-mediated neurodegenerative models. DIM protected neuronal cells against oxidative stress-induced apoptosis by regulating the expression of apoptosis-related proteins in glutamate-treated HT-22 cells. Additionally, DIM improved the expression of BDNF and antioxidant enzymes, such as heme oxygenase-1, glutamate-cysteine ligase catalytic subunit, and NAD(P)H quinine oxidoreductase-1, by promoting the activation of the TrkB/protein kinase B (Akt) pathway in the cells. Consistent with in vitro studies, DIM attenuated memory impairment by protecting hippocampal neuronal cells against oxidative damage in scopolamine-treated mice. Conclusionally, DIM exerted neuroprotective and antioxidant actions through the activation of both BDNF production and antioxidant enzyme formation in accordance with the TrkB/Akt pathway in neuronal cells. Such an effect of DIM may provide information for the application of DIM in the prevention of and therapy for neurodegenerative diseases.

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