The DOI matches its Crossref record; 88 of the 88 references it cites were found in a registry or an index.
Inflammatory Mechanisms and Oxidative Stress as Key Factors Responsible for Progression of Neurodegeneration: Role of Brain Innate Immune System
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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“Increased biomarkers of oxidative stress (Furman et al., 2016), inflammation and chronic neuroinflammation are reported to be associated with many neurodegenerative disorders of central nervous system (CNS) including AD (Leszek et al., 2016).”
From Effect of Probiotic Supplementation on Cognitive Function and Metabolic Status in Alzheimer's Disease: A Randomized, Double-Blind and Controlled Trial (2016) · cites this paper as Leszek et al., 2016
Citations
Cites
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Akbari, E., Asemi, Z., Daneshvar Kakhaki, R., Bahmani, F., Kouchaki, E., Tamtaji, O. R., Hamidi, G. A., & Salami, M. (2016) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2016.00256 · Cited by 946
“Increased biomarkers of oxidative stress (Furman et al., 2016), inflammation and chronic neuroinflammation are reported to be associated with many neurodegenerative disorders of central nervous system (CNS) including AD (Leszek et al., 2016).”
BackgroundInfluentialInflammatory Response in the CNS: Friend or Foe?
Sochocka, M., Diniz, B. S., & Leszek, J. (2017) · Molecular Neurobiology · doi:10.1007/s12035-016-0297-1 · Cited by 573
“The long-drawn release of pro-inflammatory mediators propels the inflammatory cycle by increased microglial activation and proliferation, thus stimulating enhanced release of pro-inflammatory agents [75].”
BackgroundSelf-citationTesta, G., Staurenghi, E., Zerbinati, C., Gargiulo, S., Iuliano, L., Giaccone, G., Fantò, F., Poli, G., Leonarduzzi, G., & Gamba, P. (2016) · Redox Biology · doi:10.1016/j.redox.2016.09.001 · Cited by 270
“Besides changes in oxysterol levels, it has also become evident that inflammation and oxidative stress are self-reinforcing during AD progression: inflammation can be triggered or enhanced by oxidative stress, through activation of the redox sensitive transcription factor NF-κB, and vice versa [14,23].”
BackgroundSairazi, N. S. M., & Sirajudeen, K. N. S. (2020) · Evidence-based Complementary and Alternative Medicine · doi:10.1155/2020/6565396 · Cited by 260
Oxidative Stress and the Microbiota‐Gut‐Brain Axis
Dumitrescu, L., Mitrea, I., Cozma, L., Tulbă, D., Hinescu, M. E., Ceafalan, L. C., Gherghiceanu, M., & Popescu, B. O. (2018) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2018/2406594 · Cited by 222
“There is a dual relationship between OS and inflammation: OS can be induced by inflammatory responses, and inflammation can be triggered or enhanced by ROS through activation of nuclear factor-kappa B (NF-κB), which controls the expression of many genes, including some involved in inflammatory responses leading to the…”
Background
Metadata
- Authors
- Leszek, J., E. Barreto, G., G|siorowski, K., Koutsouraki, E., Ávila-Rodrigues, M., & Aliev, G.
- 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
- 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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