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Oxidative Stress in Neurodegenerative Diseases: Molecular and Cellular Mechanisms, Therapeutic Targets and Neuroprotective Strategies

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Clinical Neurology".

Deadline for manuscript submissions: closed (30 December 2022) | Viewed by 8646

Special Issue Editor

Prof. Dr. Andrea Tarozzi

E-Mail Website
Guest Editor
Department for Life Quality Studies, University of Bologna, 40126 Bologna, Italy
Interests: neuroprotection; Parkinson’s disease; Huntington’s disease; neurodegenerative diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative stress is a common denominator of neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, and multiple sclerosis. Several studies have highlighted the interplay between oxidative stress, mitochondrial dysfunction, endoplasmic reticulum stress, proteostasis impairment and autophagy, neuroinflammation, and other neurodegenerative events. In this regard, findings of in vitro and in vivo experimental models, as well as biomarker studies in humans, have suggested a relationship between redox status regulation in neurodegenerative processes and neuroprotection. Consequently, neuroprotective molecules with antioxidant properties have received increasing attention as therapeutic and preventive interventions for neurodegenerative diseases. In this Special Issue we will focus on the latest evidence of the contribution of oxidative stress to neurodegenerative diseases, as well as novel therapeutic targets and neuroprotective strategies.

Dr. Andrea Tarozzi
Guest Editor

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Keywords

  • clinical studies;
  • translational research;
  • biomarkers of oxidative stress;
  • mechanisms of oxidative stress;
  • neurodegenerative diseases;
  • therapeutic targets;
  • antioxidant molecules;
  • neuroprotective molecules

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Published Papers (3 papers)

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Research

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15 pages, 1625 KiB  
Article
Association between Cerebrospinal Fluid Soluble TREM2, Alzheimer’s Disease and Other Neurodegenerative Diseases
by Wenchuan Zhou, Yutong Zhou and Jing Li
J. Clin. Med. 2023, 12(10), 3589; https://doi.org/10.3390/jcm12103589 - 22 May 2023
Cited by 5 | Viewed by 2276
Abstract
Background: Cerebrospinal fluid (CSF) soluble triggering receptor expressed on myeloid cells 2 (sTREM2) is a potential biomarker and therapy target for neurodegenerative diseases (NDDs). The purpose of this meta-analysis was to investigate the association between CSF sTREM2 level and NDDs, [...] Read more.
Background: Cerebrospinal fluid (CSF) soluble triggering receptor expressed on myeloid cells 2 (sTREM2) is a potential biomarker and therapy target for neurodegenerative diseases (NDDs). The purpose of this meta-analysis was to investigate the association between CSF sTREM2 level and NDDs, and to reveal the dynamic changes in CSF sTREM2 level in Alzheimer’s disease (AD) continuum. Methods: We systematically searched PubMed, Embase, Web of Science, and Cochrane Library databases for observational studies, which compared the levels of CSF sTREM2 between NDDs and controls. Sources of heterogeneity were analyzed using sensitivity analysis, subgroup analysis and meta-regression. We assessed pooled data using a random-effects model. Results: Twenty-two observational studies which included 5716 participates were identified. Compared with the controls, the whole AD continuum group showed a significant increase in CSF sTREM2 level (standardized mean difference [SMD]: 0.41, 95% confidence intervals [CI]: 0.24, 0.58, p < 0.001). The mild cognitive impairment (MCI) group displayed the largest effect size (SMD, 0.49 [95% CI: 0.10, 0.88], p = 0.014), followed by the AD cohort (SMD, 0.40 [95% CI: 0.18, 0.63], p < 0.001). The increase in sTREM2 in the preclinical stage of AD (pre-AD) group was the lowest (SMD, 0.29 [95% CI: 0.03, 0.55], p = 0.031). Other NDDs also showed an increase in the CSF sTREM2 levels compared with control groups (SMD, 0.77 [95% CI: 0.37, 1.16], p < 0.001). Conclusions: The pooled data confirmed that NDDs are associated with increased CSF sTREM2 level, thereby suggesting the CSF sTREM2 as a potential dynamic biomarker and therapy target for NDDs. Full article
(This article belongs to the Special Issue Oxidative Stress in Neurodegenerative Diseases: Molecular and Cellular Mechanisms, Therapeutic Targets and Neuroprotective Strategies)
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Review

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17 pages, 1899 KiB  
Review
Influence of Guanine-Based Purines on the Oxidoreductive Reactions Involved in Normal or Altered Brain Functions
by Mariachiara Zuccarini, Letizia Pruccoli, Martina Balducci, Patricia Giuliani, Francesco Caciagli, Renata Ciccarelli and Patrizia Di Iorio
J. Clin. Med. 2023, 12(3), 1172; https://doi.org/10.3390/jcm12031172 - 1 Feb 2023
Cited by 3 | Viewed by 2009
Abstract
The production of reactive oxygen species (ROS) in the brain is homeostatically controlled and contributes to normal neural functions. Inefficiency of control mechanisms in brain aging or pathological conditions leads to ROS overproduction with oxidative neural cell damage and degeneration. Among the compounds [...] Read more.
The production of reactive oxygen species (ROS) in the brain is homeostatically controlled and contributes to normal neural functions. Inefficiency of control mechanisms in brain aging or pathological conditions leads to ROS overproduction with oxidative neural cell damage and degeneration. Among the compounds showing therapeutic potential against neuro-dysfunctions induced by oxidative stress are the guanine-based purines (GBPs), of which the most characterized are the nucleoside guanosine (GUO) and the nucleobase guanine (GUA), which act differently. Indeed, the administration of GUO to in vitro or in vivo models of acute brain injury (ischemia/hypoxia or trauma) or chronic neurological/neurodegenerative disorders, exerts neuroprotective and anti-inflammatory effects, decreasing the production of reactive radicals and improving mitochondrial function via multiple molecular signals. However, GUO administration to rodents also causes an amnesic effect. In contrast, the metabolite, GUA, could be effective in memory-related disorders by transiently increasing ROS production and stimulating the nitric oxide/soluble guanylate cyclase/cGMP/protein kinase G cascade, which has long been recognized as beneficial for cognitive function. Thus, it is worth pursuing further studies to ascertain the therapeutic role of GUO and GUA and to evaluate the pathological brain conditions in which these compounds could be more usefully used. Full article
(This article belongs to the Special Issue Oxidative Stress in Neurodegenerative Diseases: Molecular and Cellular Mechanisms, Therapeutic Targets and Neuroprotective Strategies)
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22 pages, 15401 KiB  
Review
A Study on the Pathogenesis of Vascular Cognitive Impairment and Dementia: The Chronic Cerebral Hypoperfusion Hypothesis
by Weiwei Yu, Yao Li, Jun Hu, Jun Wu and Yining Huang
J. Clin. Med. 2022, 11(16), 4742; https://doi.org/10.3390/jcm11164742 - 14 Aug 2022
Cited by 27 | Viewed by 3442
Abstract
The pathogenic mechanisms underlying vascular cognitive impairment and dementia (VCID) remain controversial due to the heterogeneity of vascular causes and complexity of disease neuropathology. However, one common feature shared among all these vascular causes is cerebral blood flow (CBF) dysregulation, and chronic cerebral [...] Read more.
The pathogenic mechanisms underlying vascular cognitive impairment and dementia (VCID) remain controversial due to the heterogeneity of vascular causes and complexity of disease neuropathology. However, one common feature shared among all these vascular causes is cerebral blood flow (CBF) dysregulation, and chronic cerebral hypoperfusion (CCH) is the universal consequence of CBF dysregulation, which subsequently results in an insufficient blood supply to the brain, ultimately contributing to VCID. The purpose of this comprehensive review is to emphasize the important contributions of CCH to VCID and illustrate the current findings about the mechanisms involved in CCH-induced VCID pathological changes. Specifically, evidence is mainly provided to support the molecular mechanisms, including Aβ accumulation, inflammation, oxidative stress, blood-brain barrier (BBB) disruption, trophic uncoupling and white matter lesions (WMLs). Notably, there are close interactions among these multiple mechanisms, and further research is necessary to elucidate the hitherto unsolved questions regarding these interactions. An enhanced understanding of the pathological features in preclinical models could provide a theoretical basis, ultimately achieving the shift from treatment to prevention. Full article
(This article belongs to the Special Issue Oxidative Stress in Neurodegenerative Diseases: Molecular and Cellular Mechanisms, Therapeutic Targets and Neuroprotective Strategies)
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