scholarly journals Neurodegeneration: Diagnosis, Prevention, and Therapy

2021 ◽  
Author(s):  
Mrinal K. Poddar ◽  
Apala Chakraborty ◽  
Soumyabrata Banerjee
Keyword(s):  
Free Radicals ◽  
Protein Dynamics ◽  
Neurodegenerative Disorders ◽  
Defense Mechanisms ◽  
Therapeutic Strategies ◽  
Mitochondrial Dysfunctions ◽  
Abnormal Protein ◽  
Biochemical Alterations ◽  
Cellular Defense ◽  
Prevention And Therapy

Neurodegenerative disorders (NDDs) are a broad range of pathological conditions which target the neurons, creating problems in movements and mental functions. The NDDs have drawn a lot of attention among the diseases because of its complexity in causes and symptoms, lack of proper effective treatment(s), no report of irreversibility, and poor impact on social and financial aspects. Individual’s vulnerability towards the stress-related biochemical alterations including increase in oxidase enzymes’ activities and generation of free radicals, abnormal protein dynamics, mitochondrial dysfunctions, and neuroinflammation often lead to degeneration of neuronal cells. Some advanced techniques are now able to detect the development and progression of different NDDs’ complications. The current focus of research on NDDs is to establish convenient therapeutic strategies by targeting different aspects including upliftment of cellular defense mechanisms, especially oxidoreductases as a protective tool. This chapter focused on those updated information on the development, diagnosis, prevention, and therapeutic strategies of NDDs.

scholarly journals Prion protein dynamics before aggregation

2017 ◽  
Vol 114 (14) ◽  
pp. 3572-3577 ◽  
Author(s):  
Kinshuk Raj Srivastava ◽  
Lisa J. Lapidus
Keyword(s):  
Protein Dynamics ◽  
Neurodegenerative Disorders ◽  
Syrian Hamster ◽  
Time Scale ◽  
Molecular Basis ◽  
Prion Proteins ◽  
Prion Diseases ◽  
Hydrophobic Residues ◽  
Protein Deposits ◽  
Polypeptide Backbone

Prion diseases, like Alzheimer’s disease and Parkinson disease, are rapidly progressive neurodegenerative disorders caused by misfolding followed by aggregation and accumulation of protein deposits in neuronal cells. Here we measure intramolecular polypeptide backbone reconfiguration as a way to understand the molecular basis of prion aggregation. Our hypothesis is that when reconfiguration is either much faster or much slower than bimolecular diffusion, biomolecular association is not stable, but as the reconfiguration rate becomes similar to the rate of biomolecular diffusion, the association is more stable and subsequent aggregation is faster. Using the technique of Trp–Cys contact quenching, we investigate the effects of various conditions on reconfiguration dynamics of the Syrian hamster and rabbit prion proteins. This protein exhibits behavior in all three reconfiguration regimes. We conclude that the hamster prion is prone to aggregation at pH 4.4 because its reconfiguration rate is slow enough to expose hydrophobic residues on the same time scale that bimolecular association occurs, whereas the rabbit sequence avoids aggregation by reconfiguring 10 times faster than the hamster sequence.

The role of corneal crystallins in the cellular defense mechanisms against oxidative stress

2008 ◽  
Vol 19 (2) ◽  
pp. 100-112 ◽  
Author(s):  
Natalie Lassen ◽  
William J. Black ◽  
Tia Estey ◽  
Vasilis Vasiliou
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Cellular Defense

scholarly journals Antioxidative defense

2011 ◽  
Vol 65 (3-4) ◽  
pp. 247-256
Author(s):  
Jelka Stevanovic ◽  
Suncica Borozan ◽  
Slavoljub Jovic ◽  
Igor Ignjatovic
Keyword(s):  
Free Radicals ◽  
Glutathione Peroxidase ◽  
Coenzyme Q ◽  
Cellular Protein ◽  
The Body ◽  
Antioxidative Defense ◽  
Cellular Defense ◽  
Physiological Processes ◽  
Vitamins E And C ◽  
And Control

Free radicals occur constantly during metabolism and take part in numerous physiological processes, such as: intra-cellular and inter-cellular signalization, gene expression, removal of damaged or senescent cells, and control of the tone of blood vessels. However, there is an increased quantity of free radicals in situations of so-called oxidative stress, when they cause serious damage to cellular membranes (peroxidation of their lipids, damage of membrane proteins, and similar), to interior cellular protein molecules, as well as DNA molecules and carbohydrates. This is precisely why the organism has developed numerous mechanisms for removing free radicals and/or preventing their production. Some of these are enzyme-related and include superoxide-dismutase, catalase, glutathione-peroxidase, and others. Other, non-enzyme mechanisms, imply antioxidative activities of vitamins E and C, provitamin A, coenzyme Q, reduced glutation, and others. Since free radicals can leave the cell that has produced them and become dispersed throughout the body, in addition to antioxidative defense that functions within cellular structures, antioxidant extra-cellular defense has also been developed. This is comprised by: transferrin, lactoferrin, haptoglobin, hemopexin, ceruloplasmin, albumins, extra-cellular isoform SOD, extracellular glutathione-peroxidase, glucose, bilirubin, urates, and many other molecules.

scholarly journals Kynurenines in chronic neurodegenerative disorders: future therapeutic strategies

2009 ◽  
Vol 116 (11) ◽  
pp. 1403-1409 ◽  
Author(s):  
D. Zádori ◽  
P. Klivényi ◽  
E. Vámos ◽  
F. Fülöp ◽  
J. Toldi ◽  
...  
Keyword(s):  
Neurodegenerative Disorders ◽  
Therapeutic Strategies

scholarly journals Oxidative damage and cellular defense mechanisms in sea urchin models of aging

2013 ◽  
Vol 63 ◽  
pp. 254-263 ◽  
Author(s):  
Colin Du ◽  
Arielle Anderson ◽  
Mae Lortie ◽  
Rachel Parsons ◽  
Andrea Bodnar
Keyword(s):  
Oxidative Damage ◽  
Sea Urchin ◽  
Defense Mechanisms ◽  
Cellular Defense

Alternation of Mitochondrial and Golgi Apparatus in Neurodegenerative Disorders

2019 ◽  
pp. 102-128
Author(s):  
Sonia Sharma ◽  
Paramjeet Kaur ◽  
Shallina Gupta ◽  
Sushant Sharma
Keyword(s):  
Golgi Apparatus ◽  
Neurodegenerative Disorders ◽  
Morphological Changes ◽  
Mitochondrial Dysfunctions ◽  
Over Expression ◽  
Associated Proteins ◽  
Environmental Causes ◽  
Altered Proteins ◽  
Lateral Sclerosis ◽  
Apoptotic Factors

Neurodegenerative disorders (NDs) are characterized by dysfunction and loss of neurons associated with altered proteins that accumulate in the human brain and peripheral organs. Mitochondrial and Golgi apparatus (GA) dysfunctions are supposed to be responsible for various NDs. Damaged mitochondria do not produce sufficient adenosine triphosphate (ATP) and produce reactive oxygen species (ROS) and pro-apoptotic factors. Mitochondrial dysfunctions may be caused by various factors such as environmental causes, mutations in both nuclear or mitochondrial deoxyribonucleic acid (DNA), that code many mitochondrial components. Three factors that are mainly responsible for the morphological changes in GA are certain pathological conditions, drugs, and over expression of Golgi associated proteins. In this chapter, common aspects of mitochondrial and GA dysfunction concerned about NDs are summarized and described for Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and Huntington's disease (HD).

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