Cited by 206Neuroinflammation and Neurodegeneration MechanismsNeurological Disease Mechanisms and TreatmentsTryptophan and brain disorders

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Inflammatory Mechanisms and Oxidative Stress as Key Factors Responsible for Progression of Neurodegeneration: Role of Brain Innate Immune System

Leszek, Jerzy, E. Barreto, George, G|siorowski, Kazimierz, Koutsouraki, Euphrosyni, Ávila-Rodrigues, Marco, Aliev, Gjumrakch·2016·CNS & Neurological Disorders - Drug Targets

DOI 10.2174/1871527315666160202125914

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Abstract

Chronic inflammation is characterized by longstanding microglial activation followed by sustained release of inflammatory mediators, which aid in enhanced nitrosative and oxidative stress. The sustained release of inflammatory mediators propels the inflammatory cycle by increased microglial activation, promoting their proliferation and thus stimulating enhanced release of inflammatory factors. Elevated levels of several cytokines and chronic neuroinflammation have been associated with many neurodegenerative disorders of central nervous system like age-related macular degeneration, Alzheimer disease, multiple sclerosis, Parkinson's disease, Huntington' disease, and tauopathies. This review highlights the basic mechanisms of neuroinflammation, the characteristics of neurodegenerative diseases, and the main immunologic responses in CNS neurodegenerative disorders. A comprehensive outline for the crucial role of microglia in neuroinflammation and neurodegeneration and the role of Toll-like receptor signalling in coexistence of inflammatory mechanisms and oxidative stress as major factors responsible for progression of neurodegeneration have also been presented.

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Therapeutic Efficacies of Berberine against Neurological Disorders: An Update of Pharmacological Effects and Mechanisms
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“While inflammation and oxidative stress consist of distinct biochemical cascades, the processes are closely intertwined and function in parallel [154].”
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Garcinol, a multifaceted sword for the treatment of Parkinson's disease
Deb, S., Phukan, B. C., Mazumder, M. K., Dutta, A., Paul, R. K., Bhattacharya, P., Sandhir, R., & Borah, A. (2019) · Neurochemistry International · doi:10.1016/j.neuint.2019.04.004 · Cited by 46
An in silico investigation on the inhibitory potential of the constituents of Pomegranate juice on antioxidant defense mechanism: Relevance to neurodegenerative diseases
Mazumder, M. K., Choudhury, S., & Borah, A. (2019) · IBRO Reports · doi:10.1016/j.ibror.2019.05.003 · Cited by 44
“The major sources of the RONS are the NADPH oxidase, xanthine oxidase and mitochondria, and thus mitochondrial dysfunctions have been reported to cause OS and neurodegeneration in animal models of PD and AD (Beal, 2005; Jiang et al., 2016; Kim et al., 2015; Subramaniam and Chesselet, 2013; Lipski et al., 2011; Leszek…”
Background
The Role of Formyl Peptide Receptors in Neurological Diseases via Regulating Inflammation
Zhu, J., Li, L., Ding, J., Huang, J., Shao, A., & Tang, B. (2021) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2021.753832 · Cited by 44
Emerging Biosensing Technologies for Neuroinflammatory and Neurodegenerative Disease Diagnostics
Abreu, C. M., Soares-dos-Reis, R., Melo, P., Relvas, J. B., Guimarães, J., Sá, M. J., Cruz, A., & Pinto, I. M. (2018) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2018.00164 · Cited by 42
“…regulating the activity of the transcription factors AP1 and NF-κB, which in turn control the production and release of inflammatory mediators, such as the cytokines TNFα, IL-1β, IL-6, and IL-8, reactive oxygen and nitrogen species (Ortiz et al., 2013; Leszek et al., 2016; Labzin et al., 2018).”
Background
How Immune-inflammatory Processes Link CNS and Psychiatric Disorders: Classification and Treatment Implications
Anderson, G., & Maes, M. H. J. (2017) · CNS & Neurological Disorders - Drug Targets · doi:10.2174/1871527315666161122144659 · Cited by 41
Lipotoxicity, neuroinflammation, glial cells and oestrogenic compounds
Hidalgo‐Lanussa, O., Báez-Jurado, E., Echeverría, V., Ashraf, G. M., Sahebkar, A., García‐Segura, L. M., Melcangi, R. C., & Barreto, G. E. (2019) · Journal of Neuroendocrinology · doi:10.1111/jne.12776 · Cited by 42
The Contribution of Formyl Peptide Receptor Dysfunction to the Course of Neuroinflammation: A Potential Role in the Brain Pathology
Trojan, E., Bryniarska, N., Leśkiewicz, M., Regulska, M., Chamera, K., Szuster-Głuszczak, M., Leopoldo, M., Lacivita, E., & Basta‐Kaim, A. (2019) · Current Neuropharmacology · doi:10.2174/1570159x17666191019170244 · Cited by 42
Activation of FXR by ganoderic acid A promotes remyelination in multiple sclerosis via anti-inflammation and regeneration mechanism
Jia, Y., Zhang, D., Li, H., Luo, S., Xiao, Y., Li, H., Zhou, F., Wang, C., Feng, L., Wang, G., et al. (2021) · Biochemical Pharmacology · doi:10.1016/j.bcp.2021.114422 · Cited by 41
Innate Immune System Activation and Neuroinflammation in Down Syndrome and Neurodegeneration: Therapeutic Targets or Partners?
Ahmed, M. M., Johnson, N. R., Boyd, T. D., Coughlan, C. M., Chial, H. J., & Potter, H. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.718426 · Cited by 42
Selol, an organic selenium donor, prevents lipopolysaccharide-induced oxidative stress and inflammatory reaction in the rat brain
Dominiak, A., Wilkaniec, A., Jęśko, H. M., Czapski, G. A., Lenkiewicz, A. M., Kurek, E., Wroczyński, P., & Adamczyk, A. (2017) · Neurochemistry International · doi:10.1016/j.neuint.2017.02.014 · Cited by 40
“Immune activation within the central nervous system (CNS) is involved in the pathogenesis of many neurodegenerative diseases, including Alzheimer's or Parkinson's diseases as well as various neuropsychiatric disorders, like autism (Chez et al., 2007; Leszek et al., 2016; Li et al., 2009; Pasqualetti et al., 2015).”
Mutant huntingtin expression in microglia is neither required nor sufficient to cause the Huntington's disease-like phenotype in BACHD mice
Petkau, T. L., Hill, A., Connolly, C., Lu, G., Wagner, P., Kosior, N., Blanco, J., & Leavitt, B. R. (2019) · Human Molecular Genetics · doi:10.1093/hmg/ddz009 · Cited by 37
Mitochondrial dynamics and protective effects of a mitochondrial division inhibitor, Mdivi-1, in lipopolysaccharide-induced brain damage
Deng, S., Ai, Y., Gong, H., Feng, Q., Li, X., Chen, C., Liu, Z., Wang, Y., Peng, Q., & Zhang, L. (2018) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2018.01.136 · Cited by 39
Reduction of the RNA Binding Protein TIA1 Exacerbates Neuroinflammation in Tauopathy
LeBlang, C. J., Medalla, M., Nicoletti, N. W., Hays, E. C., Zhao, J., Shattuck, J. E., Cruz, A. L., Wolozin, B. L., & Luebke, J. I. (2020) · Frontiers in Neuroscience · doi:10.3389/fnins.2020.00285 · Cited by 38
Marine fungal metabolite butyrolactone I prevents cognitive deficits by relieving inflammation and intestinal microbiota imbalance on aluminum trichloride-injured zebrafish
Nie, Y., Yang, J., Zhou, L., Yang, Z., Liang, J., Liu, Y., Ma, X., Qian, Z., Hong, P., Kalueff, A. V., et al. (2022) · Journal of Neuroinflammation · doi:10.1186/s12974-022-02403-3 · Cited by 39
L-linalool exerts a neuroprotective action on hemiparkinsonian rats
de Lucena, J. D., Gadelha-Filho, C. V. J., da Costa, R. O., de Araújo, D. P., Lima, F. A. V., Neves, K. R. T., & Viana, G. S. D. B. (2020) · Naunyn-Schmiedeberg s Archives of Pharmacology · doi:10.1007/s00210-019-01793-1 · Cited by 42
“In conclusion, considering that neuroinflammation and oxidative stress play key roles on the neuropathological features of PD (Mosley et al. 2006; Taylor et al. 2013; Leszek et al. 2016) and that LIN exerts both anti-inflammatory and antioxidant actions, our results strongly suggest that LIN neuroprotective activity i…”
Time-Dependent Protective and Pro-Resolving Effects of FPR2 Agonists on Lipopolysaccharide-Exposed Microglia Cells Involve Inhibition of NF-κB and MAPKs Pathways
Tylek, K., Trojan, E., Leśkiewicz, M., Regulska, M., Bryniarska, N., Curzytek, K., Lacivita, E., Leopoldo, M., & Basta‐Kaim, A. (2021) · Cells · doi:10.3390/cells10092373 · Cited by 37
KCa3.1 deficiency attenuates neuroinflammation by regulating an astrocyte phenotype switch involving the PI3K/AKT/GSK3β pathway
Wei, T., Wang, Y., Xu, W., Liu, Y., Chen, H., & Yu, Z. (2019) · Neurobiology of Disease · doi:10.1016/j.nbd.2019.104588 · Cited by 33
Alzheimer’s disease: review of current nanotechnological therapeutic strategies
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“Therefore, these data indicate that the resolution of inflammatory response is a multistage and active process [50], and the failure of one or more steps may be involved in the prolonged inflammation and the pathogenesis of chronic inflammatory diseases due to constant stimulation of the immune system, increased pro-i…”
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The Neuroprotective Effect of Conditioned Medium from Human Adipose-Derived Mesenchymal Stem Cells is Impaired by N-acetyl Cysteine Supplementation
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“Nowadays, neuroinflammation, along with one of its main intrinsic features, oxidative stress, is considered one of most important pathophysiological explanations for the development and progression of neurodegenerative diseases [1, 2].”
Background
Is cerebral glucose metabolism related to blood–brain barrier dysfunction and intrathecal IgG synthesis in Alzheimer disease?
Chiaravalloti, A., Fiorentini, A., Ursini, F., Martorana, A., Koch, G., Belli, L., Toniolo, S., Pietro, B. D., Motta, C., & Schillaci, O. (2016) · Medicine · doi:10.1097/md.0000000000004206 · Cited by 32
“On the other side, the identification of intratechal-synthesized Ig could represent only the epiphenomenon of the presence of deranged immune cells inside the CNS, and these cells contributing to neuropathology with Ig-independent mechanisms.([15]) Contrarily to Qalb, the percentage of AD subjects showing alterations…”
Background
Differential Modulation of NF-κB in Neurons and Astrocytes Underlies Neuroprotection and Antigliosis Activity of Natural Antioxidant Molecules
Martorana, F., Foti, M., Virtuoso, A., Gaglio, D., Aprea, F., Latronico, T., Rossano, R., Riccio, P., Papa, M., Alberghina, L., et al. (2019) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2019/8056904 · Cited by 31
“Nevertheless, chronic astrocytic activation (reactive gliosis) may hold deleterious consequences that limit functional repair of brain parenchyma [4, 6, 7].”
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Anti-oxidative activity of probiotics; focused on cardiovascular disease, cancer, aging, and obesity
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Tanshinone IIA attenuates Aβ-induced neurotoxicity by down-regulating COX-2 expression and PGE2 synthesis via inactivation of NF-κB pathway in SH-SY5Y cells
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“Microglial activation is a central component of the neuroinflammatory cascade leading to cognitive decline in AD [69].”
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Putative neural consequences of captivity for elephants and cetaceans
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“One neural consequence under such conditions is microglia activation and a sustained release of inflammatory mediators (Leszek et al. 2016).”
Background
Taurine counteracts the neurotoxic effects of streptozotocin-induced diabetes in rats
Caletti, G., Herrmann, A. P., Pulcinelli, R. R., Reinhardt, L. S., Morás, A. M., Vianna, P., Chies, J. A. B., Moura, D. J., Barros, H. M. T., & Gomez, R. (2017) · Amino Acids · doi:10.1007/s00726-017-2495-1 · Cited by 25
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Oxidative Stress Assessment in Alzheimer’s Disease: A Clinic Setting Study
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“Axonal loss and glial swelling are prominent features of AD (Englund, 1998; Stokin et al., 2005), this may lead to the enlarged perivascular spaces in the pathogenesis of AD (Fischer & Maier, 2015; Kawahara, 2010; Leszek et al., 2016; Reddy, 2009; Santos et al., 2010; Shu et al., 2013).”
Cotinine: A Therapy for Memory Extinction in Post-traumatic Stress Disorder
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“On the other hand, inflammation can be triggered or enhanced by oxidative stress through activation of nuclear factor-kappa B (NF-kB), which controls the expression of many genes, including inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX2), which are involved in proinflammatory cytokine production (68…”
Background
Probiotics that Ameliorate Cognitive Impairment through Anti-Inflammation and Anti-Oxidation in Mice
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“ROS can also trigger or enhance inflammation through direct activation of NF-κB (Leszek et al. 2016).”
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“A relationship between oxidative stress and neuroinflammation and their contribution in neurodegeneration have been widely suggested [64,65].”
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The human body as an energetic hybrid? New perspectives for chronic disease treatment?
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“This observation links oxidative stress with the development of neuronal death and neural dysfunction [16, 17].”
Background

Authors: Leszek, J., E. Barreto, G., G|siorowski, K., Koutsouraki, E., Ávila-Rodrigues, M., & Aliev, G.
ORCID: Leszek, Jerzy
Aliev, Gjumrakch
Venue: CNS & Neurological Disorders - Drug Targets
Publisher: Bentham Science Publishers Ltd.
Published: 2016-03-10
Volume: 15
Issue: 3
Pages: 329-336
ISSN: 1568-007X (ISSN-L)
1871-5273
DOI: 10.2174/1871527315666160202125914
OpenAlex: W2271123303
Semantic Scholar: 91475bee1cf3d32abe2d7e1be1755b559ca3dc93
Cited by: 206
References: 88
Citations by year: 2026: 13 · 2025: 19 · 2024: 23 · 2023: 16 · 2022: 13 · 2021: 23 · 2020: 20 · 2019: 16 · 2018: 31 · 2017: 23 · 2016: 9
FWCI: 14.41
Type: journal article
Language: en
Open access: closed
Locations: CNS & Neurological Disorders - Drug Targets (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Keywords: neuroinflammation, neurodegeneration, microglial activation, oxidative stress, nitrosative stress, Toll-like receptor signaling, cytokines, Alzheimer's disease, Parkinson's disease, Huntington's disease, multiple sclerosis, age-related macular degeneration, tauopathy
MeSH terms: Animals, Brain, Humans, Immunity, Innate, Inflammation, Cytokines, Microglia, Oxidative Stress, Disease Progression, Neurodegenerative Diseases

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Inflammatory Mechanisms and Oxidative Stress as Key Factors Responsible for Progression of Neurodegeneration: Role of Brain Innate Immune System

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