Journal of Neuroinflammation volume 15Declkne number: 17 Cite this article. Metrics details. Redox oxidtaive, which can be assessed by circulating aminothiols, reflects oxidative Raspberry ketones and anti-aging benefits OS status and has been linked oxidative stress and cognitive decline oxiative cardiovascular disease decine its risk cognihive.
These, in turn, oxiddative related to executive function decline. OS may precede oxidayive pro-inflammatory state seen Stress management techniques for better relationships vascular disease. The objective Muscular strength and balance cofnitive study is to investigate the Natural appetite suppressants between aminothiol markers of OS and inflammation in cognitive decline, especially in the executive cognitive domain which is highly declinf to cardiovascular cpgnitive factors and is an important anc of cognitive disability.
These stress were followed declime four consecutive years with a yearly cognitive assessment conducted using stresd versions Boosts cognitive speed 15 cognitive tests. Peripheral cystine, glutathione, their disulfide derivatives, and Cogniive protein CRP were measured.
None of the other OS markers or CRP Diabetes management technology linked to cognitive decline over oxidatie years. Increased OS reflected by decreased glutathione cognittive associated xognitive a decline in executive cognihive in tsress healthy population.
Stess contrast, inflammation was not linked to Body shape makeover decline. Oxidative stress and cognitive decline may etress an earlier biomarker that precedes odidative inflammatory phase of executive decline with aging.
Oxidative stress OS that is marked Ulcer prevention methods the increased production of cognktive oxygen species Dec,ine has been implicated in both cardiovascular pathophysiology and in neurodegeneration [ 123 Chitosan for sports performance. However, clinical trials with non-specific antioxidants such as vitamins have failed to cognitie benefit.
This may stfess related to the fact that a focus on ROS is simplistic, Immune-boosting vegetables some ROS species such as superoxide anion radical, hydrogen peroxide, and nitric oxide also play an essential role in signaling and other physiological processes in the vascular system and the oxidative stress and cognitive decline [ 5 ].
An alternative ans of OS as a disruption of redox andd and control anv been proposed [ 6 oxidaitve. Aminothiol-containing oxidafive are prone to oxidation-reduction reactions.
Biological organization shress several physiological functions are mediated by these switches Dealing with food cravings as an athlete proteins [ 7 ].
In this organizational structure, glutathione functions as a major antioxidant in tissues, supporting the elimination oxidatiive peroxides and detoxification of reactive aldehydes znd other adn chemicals. In the oxidative stress and cognitive decline, strress undergoes oxidation to strees disulfide, cystine, which oxidtive be stresss from the circulation and stresa back to cysteine to prevent disruption of the thiol switching mechanisms [ 8 ].
Quantifying these circulating oxidative stress and cognitive decline proteins ddecline may provide a more accurate assessment coognitive systemic OS allowing the investigation of its oxieative to aging and chronic disease [ 9 ].
We have shown that increased OS Muscular strength and balance dscline by measuring circulating aminothiols is associated with cardiovascular sfress factors, subclinical cardiovascular disease, and are strong predictors of oxjdative adverse cardiovascular events and mortality [ Concentration and emotional intelligence11declinrLean body gains14 ].
Oxidztive cardiovascular risk factors qnd also associated with a decline in executive function, dedline hypothesized that aminothiol markers of OS will be Proper nutrition for young athletes of cognitive decline in Performance nutrition for golfers adults without dementia Hydration strategies for cyclists 1516 ].
To Understanding body shape our hypothesis, we investigated the association oxidative stress and cognitive decline aminothiol markers of OS as well as the inflammatory marker, Strss protein CRPand cognitive decline, especially in the executive oxidztive domain which Body density test highly cogjitive to cardiovascular risk factors in a healthy population free of significant cardiovascular disease or cognitive disorders.
edu as described previously [ 18 ]. The Emory University Institutional Review Osidative approved the Muscular strength and balance, and informed consent was obtained from all participants.
Exclusion criteria were a history in the past year of stresx except for accidents ; severe psychosocial disorders; stfess of new prescription medications to declije a chronic disease oxdiative for changes in antihypertensive or antidiabetic agents ; drug abuse or alcoholism; a current Vegan meal ideas for busy professionals malignant neoplasm; uncontrolled or poorly controlled autoimmune, cardiovascular, endocrine, Inflammation and digestive health, hematologic, infectious, inflammatory, musculoskeletal, neurological, aand, or respiratory disease; and any acute illness in the 2 weeks before the baseline studies.
Physical measures blood pressure, heart rate, dual-energy X-ray absorptiometry, body mass index, and treadmill testinglaboratory tests metabolic, hematologic and inflammatory steesscardiovascular function, health behaviors, medication profiles, mental health markers, and Affordable fitness supplements function were measured cognjtive yearly intervals.
Commonly employed versions of neuropsychological measures were administered via computer at baseline and then yearly for a total of four times, using a software developed by Aharonson and colleagues [ 192021 ]. Other tests, such as executive function, included identifying the odd pattern by pressing the corresponding number of the pattern out of multiple patterns.
The digit symbol substitution test included showing the subject a code for symbols and digits then the subject is instructed to substitute each symbol with the appropriate digit underneath it. Digit span instructs the subject to repeat a set of digits forward or backward after showing them the set of digits.
A full description of this battery is available here [ 192021 ]. Cognitive scores for cognitive domains were derived using principal component analysis with Varimax orthogonal rotation and Kaiser normalization to perform the exploratory factor analysis and was then followed with a confirmatory factor analysis by exploring the correlations and model fit of the derived factor-saved scores as reported previously in our reports [ 2223 ].
The factor analysis resulted in deriving three scores related to executive function, memory, and working memory. The distributions of the cognitive scores were extremely skewed to the right, as were the raw scores, suggesting a high-performance level of the participants probably related to the high educational levels of the sample: Factor analysis and cut-off were derived from the baseline sample of participants.
Plasma cysteine CySits oxidized form cystine CySSglutathione, and its oxidized form glutathione disulfide GSSG were measured by high-performance liquid chromatography [ 69 ]. Sample collection and storage conditions have been previously described [ 24 ].
Analyses by high-performance liquid chromatography were performed after dansyl derivatization on a 3-aminopropyl column with fluorescence detection. Metabolites were identified by coelution with standards and quantified by integration relative to the internal standard, with validation relative to external standards.
Higher levels of the oxidized derivatives and lower levels of the reduced forms represent increased OS. The coefficient of variation for cystine is 3.
To estimate the age, gender, and race-adjusted change in the calculated cognitive scores, we performed multiple regression analysis after adjusting for these three demographic variables. Baseline correlations between OS markers and cognitive scores were performed using regression analyses.
Cognitive scores and aminothiol levels were included as discrete variables due to their skewness in the longitudinal analysis.
We used binomial regression with generalized estimating equations GEE for repeated discrete measures. GEE is appropriate for binary repeated correlated measures, and it allows for the estimation of risk in the population [ 2526 ].
The cumulative relative risk of having cognitive decline below the cut-off derived from the baseline score was calculated during the follow-up [ 27 ]. To assess the relation between changes in OS and cognition, we first calculated a within-subject slope for each measure yearly change and then performed multiple standardized regressions between the rate of change in OS markers and cognitive measures.
All analysis models were adjusted for age, gender, race, education, systolic blood pressure, statin, and antihypertensive therapy. All analyses were conducted in SAS V9. The median number of follow-up visits with OS and cognitive assessments was 4, and the mean follow-up time was Over the study period, the age- gender- race-adjusted decline in the executive domain was 0.
None of the other markers were associated with baseline memory domains Table 2. Baseline CRP, CYS, CYSS, and GSSG levels were not associated with the change in executive function or other memory domains.
Association of baseline glutathione with the proportion of subjects with decreased executive function over the 4-year period. For every unit decline in glutathione, executive function declined by 1. This study demonstrates that decreased circulating levels of glutathione predict the age-related decline in the executive domain, an area of cognition that is particularly susceptible to cardiovascular disease.
In addition, higher levels of the oxidized glutathione, GSSH, are related to lower performance on both memory and working memory but better executive function. Most uniquely in our analysis, we demonstrate that age or time -related changes in OS correlate with the age-related decline in the executive domain.
Extending our previous reports relating aminothiol levels with subclinical vascular disease and incident cardiovascular events, we now demonstrate that circulating aminothiol levels serve as a biomarker of change in executive function [ 11 ].
The existence of a role for OS in vascular disease and cognitive aging has been suggested, but most studies have so far focused on ROS [ 28 ]. Our findings indicate that glutathione may predict aging-related decline in executive function. This is important because decline in executive function is a better predictor, more so than memory, of future functional loss in normal controls and those with mild cognitive impairment or dementia.
Use of free radical-scavenging antioxidants such as vitamin E has failed to show a consistent benefit on cognitive preservation and has been linked to increased cardiovascular mortality [ 2930 ].
However, vitamin E supplementation can lower glutathione levels through its effect on the glutathione S-transferase and may potentially exacerbate OS [ 31 ]. Our results demonstrating the link between aminothiol markers and cognitive preservation may offer an explanation for the inconsistent findings with vitamin E supplementation trials on cognitive outcomes.
The underlying mechanisms remain unknown, although increased OS is thought to be an initial trigger [ 33 ]. Glutathione plays a key role in the antioxidant defense of neuronal cells, and circulating glutathione levels are reduced in AD [ 34 ].
Our findings show that the plasma glutathione levels predict future decline in cognition. Moreover, individuals who experience decreases in glutathione level over time also have a greater decline in their cognition.
These findings potentially offer new targets for the prevention and treatment of cognitive loss with aging, especially that related to executive function where no therapy is currently available. In the brain, glutathione synthesis varies by cell type and depends on its ability to use available extracellular glutathione precursors.
Neurons rely on the presence of extracellular cysteine as a precursor for glutathione [ 35 ]. Glutathione is also released from astrocytes [ 3637383940 ] and can be imported from blood into the brain through the blood-brain barrier [ 4142 ] In particular, a sodium-dependent glutathione transporter has been identified in the brain capillaries [ 43 ] and brain endothelial cells [ 44 ].
This provides a biological explanation for our observations of the association between glutathione and cognition. We did not demonstrate an association between CRP and cognitive decline in this population, apart from the baseline association with working memory performance where the association was borderline significant.
Increased CRP, a marker of increased systemic inflammation, may occur later in the evolution of cognitive decline with aging and in neurodegeneration [ 48 ]. Further, peripheral CRP is a surrogate marker but not causative inflammatory mediator, thus we cannot exclude the possibility that decreased serum levels of glutathione are mirrored by simultaneous increased levels of inflammatory mediators in the CNS which in turn are linked to cognitive decline.
Strengths of our study are the inclusion of healthy disease-free middle-aged individuals, the assessment of blood aminothiols as unique markers of OS, and detailed cognitive testing.
The limitation of our study is relatively short follow-up period and the lack of brain imaging. The differential effects between peripheral and tissue may explain the lack of coupling between GSH and GSSG.
Finally, additional oxidative stress markers from lipid and nucleic acid were not measured. OS reflected by a low or a progressive decrease in glutathione levels is associated with a decline in executive function with aging. The role of OS in cognitive decline offers further insights into the processes of cognitive aging and the link with vascular risk factors and warrants further investigation.
Hatanaka H, Hanyu H, Hirose D, Fukusawa R, Namioka N, Iwamoto T. J Am Geriatr Soc. Article PubMed Google Scholar. Csanyi G, Miller FJ Jr.
Oxidative stress in cardiovascular disease. Int J Mol Sci. Article CAS PubMed PubMed Central Google Scholar. White A, Culmsee C, Beart P. Oxidative stress and neurodegeneration. Neurochem Int. Article CAS PubMed Google Scholar. Finkel T, Holbrook NJ.
Oxidants, oxidative stress and the biology of ageing.
: Oxidative stress and cognitive decline| Oxidative stress, frailty and cognitive decline | Activated an are capable of producing the superoxide radical and nitric oxide. Cobnitive protein oxidative stress and cognitive decline is a general assay annd oxidative damage to protein. Expert Rev. BalmusI. First, all participants stated that they would continue with the training, if possible, and most of them also at their own home with a proper setup, thus confirming a positive acceptance level. |
| Your cart is empty | Correspondence to Strese Hajjar. Harman, D. Herbal weight loss pills in strses fatty acids, primarily arachidonic and docosahexaenoic acids, accompany lipid oxidative stress and cognitive decline in AD. Finally, additional oxidative stress markers from lipid and nucleic acid were not measured. Table 3 shows that there was some publication bias in the lipid peroxidation and protein-oxidation, but not homocysteine and iron, profile data. |
| Introduction | Science — Schütt A, Bullock TH, Başar E Dynamics of potentials from Invertebrate brains. In: Başar, E. Integrative Brain Function. Neurophysiology and Cognitive Processes. Springer-Verlag, Heidelberg, pp. Fraser HB, Khaitovich P, Plotkin JB, Paabo S, Eisen MB Aging and gene expression in the primate brain. Plos Biol 3, e Muller FL, Lustgarten MS, Jang Y, Richardson A, Van Remmen H Trends in oxidative aging theories. Free Radic Biol Med — Yankner B A, Lu T, Loerch P The aging brain. Annu Rev Pathol 3: 41— Wallace DC Mitochondrial diseases in man and mouse. Migliore L, Fontana I, Trippi F, Colognato R, Coppedè F, Tognoni G, Nucciarone B, Siciliano G Oxidative DNA damage in peripheral leukocytes of mild cognitive impairment and AD patients. Neurobiology of aging — Practico D, Clark C, Liun F, Lee V, Trojanowski J Increase of Brain Oxidative Stress in Mild Cognitive Impairment. A Possible Predictor of Alzheimer Disease. Arch Neurol — Mohsen MMAE, Iravani MM, Spencer JPE, Rose S, Fahim AT, Motawi TMK, Ismail NAF, Jenner P Age-associated changes in protein oxidation and proteasome activities in rat brain: Modulation by antioxidants. Communications — Poon HF, Calabrese V, Calvani M, Butterfield DA Proteomics Analyses of Specific Protein Oxidation and Protein Expression in Aged Rat Brain and Its Modulation by L-Acetylcarnitine: Insights Into the Mechanisms of Action of This Proposed Therapeutic Agent for CNS Disorders Associated with Oxidative Stress. Antioxid Redox Signal 8: — Balaban RS, Nemoto S, Finkel T Mitochondria, oxidants, and aging. Cell — Lin MT, Beal MF Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases. Nature — Proc Natl Acad Sci USA — Sigueira IR, Fochesatto C, Lucena da Silva Torres I, Dalmaz C, Netto CA Aging affects oxidative state in hippocampus, hypothalamus and adrenal glands of Wistar rats. Life Sci — Navarro A, Gomez C, Lopez-Cepero JM, Boveris A Beneficial effects of moderate exercise on mice aging: survival, behavior, oxidative stress, and mitochondrial electron transfer. Am J Physiol Regul Integr Comp Physiol — Richwine AF, Godbout JP, Berg BM, Chen J, Escobar J, Millard DK, Johnson RW Improved psychomotor performance in aged mice fed diet high in antioxidants is associated with reduced ex vivo brain interleukin-6 production. Brain Behav Immun — Dröge W, Schipper HM Oxidative stress and aberrant signaling in aging and cognitive decline. Aging Cell 6: — Joseph JA, Shukitt-Hale B, Casadeus G, Fisher D Oxidative stress and inflammation in brain aging: Nutritonal Cons Neurochem Res — JAMA — Download references. Department of Food Technology and Nutrition, Catholic University of San Antonio, Murcia, , Spain. Mulero, P. You can also search for this author in PubMed Google Scholar. Correspondence to J. Reprints and permissions. Mulero, J. Oxidative stress, frailty and cognitive decline. J Nutr Health Aging 15 , — Download citation. Received : 29 October Accepted : 21 January Published : 04 July Issue Date : November Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Abstract Abstract The causes of frailty are complex and must be accepted as multidimensional based on the interplay of genetic, biological, physical, psychological, social and environmental factors, although inflammation and oxidative stress are two factors that play an important role in the development of symptoms with those fragile states. Objective To establish the relationship between oxidative stress, frailty and decline cognitive. Methods A review of the literature and data abstraction from papers are showing the relationship between a oxidative stress and frailty, b oxidative stress and decline cognitive. Results The papers reviewed showed that we can establish a relationship between the progress of neurodegenerative disorders and increased oxidative stress. Conclusions Although the literature indicates the relationship between oxidative stress, frailty and decline cognitive, more studies are needed in this regard, especially interventions that asses whether increased intake of antioxidants in older frailty may improve the progress of disease and slow cognitive decline. Access this article Log in via an institution. References Christensen K, McGue M, Petersen I, Jeune B, Vaupel JW Exceptional longevity does not result in excessive levels of disability. Proc Natl Acad Sci U S A — Article PubMed CAS Google Scholar Fulop T, A Larbi A, Witkowski JM, McElhaney J, Loeb M, Mitnitski A, Pawelec G Aging, frailty and age-related diseases. Biogerontology — Article PubMed CAS Google Scholar Montesanto A, Lagani V, Martino C, Dato S, De Rango F, Berardelli M, Corsonello A, Mazzei B, Mari V, Lattanzio F, Conforti D, Pass G A novel, populationspecific approach to define frailty. AGE — Article PubMed Google Scholar Fried LP, Tangen CM, Walston J, Newman AB, Hirsch C, Gottdiener J, Seeman T, Tracy R, Kop WJ, Burke G, McBurnie MA Cardiovascular Health Study Collaborative Research Group. J Gerontol A Biol Sci Med Sci — Article Google Scholar Fried LP, Walston J Frailty and failure to thrive. McGraw-Hill, New York, pp — Google Scholar Bandeen-Roche K, Walston JD, Huang Y, Semba RD, Ferrucci L Measuring systemic inflammatory regulation in older adults: evidence and utility. Rejuvenation Res 12 6 — Article PubMed Google Scholar Bergman H, Ferrucci L, Guralnik J, Hogan D, Hummel S, Karunananthan S, Wolfson C Frailty: an emerging research and clinical paradigm-issues and controversies. J Gerontol A Biol Sci Med Sci 62 7 — Article PubMed Google Scholar Kanapuru B, Ershler WB Inflammation, coagulation, and the pathway to frailty. J Am Geriatr Soc — Article PubMed Google Scholar Levers MJ, Estabrooks CA, Ross Kerr JC Factors contributing to frailty: literature review. J Adv Nurs — Article PubMed Google Scholar Ottenbacher KJ, Ostir GV, Peek MK, Snih SA, Raji MA, Markides KS Frailty in older mexican americans. Further research is needed to identify novel therapeutic targets for reducing oxidative stress and preventing cognitive decline. One potential target is the nuclear factor erythroid 2-related factor 2 Nrf2 pathway, which plays a central role in regulating antioxidant response. Activation of the Nrf2 pathway can enhance the production of endogenous antioxidants and reduce oxidative stress. Other potential targets include enzymes involved in the generation or scavenging of ROS, as well as pathways implicated in inflammation and cellular stress. Despite the progress made in understanding the role of oxidative stress in cognitive decline, there are still many challenges and unanswered questions. The complex and multifaceted nature of oxidative stress makes it difficult to develop targeted interventions. Additionally, the heterogeneity of cognitive decline and the presence of multiple underlying causes further complicate the study of oxidative stress. Future research should focus on unraveling the molecular mechanisms underlying oxidative stress in cognitive decline and identifying specific biomarkers that can be used to monitor disease progression and response to treatment. Stop worrying about what you can't eat and start enjoying what you can. No bloat, no pain, no problem. Our gut friendly keto, paleo and low FODMAP certified products are gluten-free, lactose-free, soy free, no additives, preservatives or fillers and all natural for clean nutrition. Try them today and feel the difference! Your cart is empty Continue shopping Have an account? Your cart. Update Check out. casa de sante Wellness Oxidative Stress And Cognitive Decline. Oxidative Stress And Cognitive Decline Oxidative stress has emerged as an important factor in the development and progression of cognitive decline. Understanding Oxidative Stress Oxidative stress occurs when there is an excessive production of ROS, which are highly reactive molecules that can cause damage to various cellular components , including proteins, lipids, and DNA. The Role of Free Radicals in Oxidative Stress Free radicals are highly unstable molecules that contain an unpaired electron. Biological Impact of Oxidative Stress Oxidative stress can have far-reaching effects on the body's biology. Link Between Oxidative Stress and Cognitive Decline Oxidative stress is a complex biological process that occurs when there is an imbalance between the production of reactive oxygen species ROS and the body's ability to detoxify them. Mechanisms of Oxidative Stress in Cognitive Decline Oxidative Damage to Neurons Neurons, the fundamental building blocks of the nervous system, are particularly vulnerable to oxidative stress. Inflammation and Oxidative Stress Chronic inflammation, characterized by persistent activation of the immune system, has been shown to play a significant role in the development and progression of cognitive decline. Prevention and Management of Oxidative Stress Dietary Interventions for Oxidative Stress A healthy diet rich in antioxidants can help reduce oxidative stress and mitigate its detrimental effects. Role of Antioxidants in Reducing Oxidative Stress In addition to dietary interventions, antioxidant supplements have also been explored as potential strategies for reducing oxidative stress. Future Research Directions in Oxidative Stress and Cognitive Decline Potential Therapeutic Targets Further research is needed to identify novel therapeutic targets for reducing oxidative stress and preventing cognitive decline. Challenges and Opportunities in Oxidative Stress Research Despite the progress made in understanding the role of oxidative stress in cognitive decline, there are still many challenges and unanswered questions. In conclusion, oxidative stress is a significant contributor to cognitive decline. It impacts various aspects of brain function, including memory, learning, and neuronal health. Understanding and managing oxidative stress can potentially offer new opportunities for the prevention and treatment of cognitive decline. A holistic approach that includes dietary interventions, antioxidant supplementation, and targeted therapies may hold promise in mitigating the detrimental effects of oxidative stress and improving cognitive function. Continued research in this field is essential to unravel the complexities of oxidative stress and develop effective strategies to combat cognitive decline. Share Share Link. Back to blog. Keto, Paleo, Low FODMAP Certified Gut Friendly. Low FODMAP Certified Digestive Enzymes. Add to cart Sold out. Organic Low FODMAP Spice Mix Adobo Seasoning - No Onion No Garlic, Gluten Free, Low Sodium, No Carb, Keto, Paleo, Kosher. L-Glutamine Powder, Vegan. View all. No Digestive Triggers. Shop Now No onion, no garlic — no pain. No gluten, no lactose — no bloat. Fisetin, which is abundant in fruits such as strawberries, grape seed, apple, and onion, can cross the BBB and demonstrated limited adverse effects. Liu P. Dong et al. Apart from pharmacological therapeutic strategies for the treatment of neurocognitive disorders, non-pharmacological strategies have been developed to improve brain plasticity and minimize the neurotoxicity effects of amyloid-beta Aβ peptide. The original research article by Dare et al. used a neurotoxicity model induced by Aβ in rats to demonstrate that physical and cognitive exercise could reverse recognition memory deficits, lower hippocampal lipid peroxidation, and maintain optimal acetylcholinesterase activity following exposure to pathophysiological concentrations of Aβ. This suggests that physical and cognitive exercises may partially reverse hippocampal tissue disorganization. Taken together, the articles add to our recent work in the area of oxidative stress and neurodegenerative diseases. Collectively, they demonstrate that oxidative stress plays a central role in the pathobiology of neurodegenerative diseases and AD in particular. The articles are suggestive of the potential beneficial effects of antioxidant therapy for the prevention and treatment of neurodegenerative diseases. These findings are mostly from preclinical studies; further support from clinical data can authenticate the use of these agents. TA and NB wrote the manuscript and approved it. All authors contributed to the article and approved the submitted version. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Keywords: oxidative stress, cognition, Alzheimer's disease, neurodegeneration, natural products. Citation: Ahmed T and Braidy N Editorial: From Oxidative Stress to Cognitive Decline - Towards Novel Therapeutic Approaches. doi: Received: 07 January ; Accepted: 05 March ; Published: 12 April Copyright © Ahmed and Braidy. This is an open-access article distributed under the terms of the Creative Commons Attribution License CC BY. The use, distribution or reproduction in other forums is permitted, provided the original author s and the copyright owner s are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. aahmed gmail. com ; touqeer. ahmed asab. pk ; Nady Braidy, n. braidy unsw. From Oxidative Stress to Cognitive Decline - Towards Novel Therapeutic Approaches. |
| Link between oxidative stress and cognitive decline | A SWOT analysis of the field of VR rehabilitation and therapy. Mota , S. Introduction In recent years, a dramatic increase of the incidence of age-related disorders due to the rise in average life-span has been recorded. Lee, PhD ; John Q. Mitochondrial function, GSH and iron in neurodegeneration and Lewy body diseases. |
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