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Neuroinflammation, Oxidative Stress and the Pathogenesis of Alzheimers Disease
Abstract
Alzheimers disease (AD) is the most common neurodegenerative disorder that affects the elderly. The increase of lifeexpectancy is transforming AD into a major health-care problem. AD is characterized by a progressive impairment of memory and other cognitive skills leading to dementia. The major pathogenic factor associated to AD seems to be amyloid-beta peptide (Aβ) oligomers that tend to accumulate extracellularly as amyloid deposits and are associated with reactive microglia and astrocytes as well as with degeneration of neuronal processes. The involvement of microglia and astrocytes in the onset and progress of neurodegenerative process in AD is becoming increasingly recognized, albeit it is commonly accepted that neuroinflammation and oxidative stress can have both detrimental and beneficial influences on the neural tissue. However, little is known about the interplay of microglia, astrocytes and neurons in response to Aβ, especially in the early phases of AD. This review discusses current knowledge about the involvement of neuroinflammation in AD pathogenesis, focusing on phenotypic and functional responses of microglia, astrocytes and neurons in this process. The abnormal production by glia cells of pro-inflammatory cytokines, chemokines and the complement system, as well as reactive oxygen and nitrogen species, can disrupt nerve terminals activity causing dysfunction and loss of synapses, which correlates with memory decline; these are phenomena preceding the neuronal death associated with late stages of AD. Thus, therapeutic strategies directed at controlling the activation of microglia and astrocytes and the excessive production of pro-inflammatory and pro-oxidant factors may be valuable to control neurodegeneration in dementia. Keywords: Amyloid-beta, microglia, astrocytes, neurons, pro-inflammatory factors, reactive oxygen species, neurodegeneration, Alzheimer's disease, Dementia, Neuroinflammation, Pro-oxidant factors, Memory, Mild cognitive impairment, CNS, cytokines, prostaglandins, IL-1, PPAR-g, Complement system, Amyloid pla, Trophic factors, Glia-derived neurotrophic factor, Glial scars, Ca2+ overload, Homeostasis, Antioxidants, Electron transport chain, Curcumin, Quercetin
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“Finally, they have an impact on the unsaturated fatty acids chain of membrane phospholipids, causing cell lysis [116,117,118].”
From Multi-Target Mechanisms of Phytochemicals in Alzheimer’s Disease: Effects on Oxidative Stress, Neuroinflammation and Protein Aggregation (2022) · cites this paper as [117]
In the citing paper
“This immune response causes both an invasion of the glia by circulating immune cells and the production of pro-inflammatory cytokines, tumor necrosis factor (TNF)-α, interleukin (IL) IL-1β and IL-6-, nitric oxide (NO), prostaglandin E2 (PGE2), chemokines, and ROS.”
From Multi-Target Mechanisms of Phytochemicals in Alzheimer’s Disease: Effects on Oxidative Stress, Neuroinflammation and Protein Aggregation (2022) · cites this paper as [117]
In the citing paper
“AD is also induced by neuroinflammation processes that occur as a brain immune barrier [117,154].”
From Multi-Target Mechanisms of Phytochemicals in Alzheimer’s Disease: Effects on Oxidative Stress, Neuroinflammation and Protein Aggregation (2022) · cites this paper as [117]
In the citing paper
“Oxidative stress associated with Aβ pathology plays an important role in the death of neurons in the AD brain [82,83,84,85].”
From Centella Asiatica Improves Memory and Promotes Antioxidative Signaling in 5XFAD Mice (2019) · cites this paper as [82]
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Metadata
- Authors
- Agostinho, P., A. Cunha, R., & Oliveira, C.
- Affiliations
- University of Coimbra (PT)
- Corresponding author
- Oliveira, Catarina
- Venue
- Current Pharmaceutical Design
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2010-08-01
- Volume
- 16
- Issue
- 25
- Pages
- 2766-2778
- ISSN
- 1381-6128 (ISSN-L)
- OpenAlex
- W2114324710
- Cited by
- 685
- References
- 0
- Citations by year
- 2026: 35 · 2025: 44 · 2024: 46 · 2023: 43 · 2022: 52 · 2021: 61 · 2020: 58 · 2019: 42 · 2018: 44 · 2017: 51 · 2016: 32 · 2015: 36 · 2014: 34 · 2013: 37 · 2012: 41
- FWCI
- 20.75
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Pharmaceutical Design (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- Alzheimer's disease, neuroinflammation, oxidative stress, amyloid-beta oligomers, amyloid plaques, microglia, astrocytes, neurodegeneration, inflammatory cytokines, chemokines, complement system, reactive oxygen species, reactive nitrogen species, synaptic loss, memory impairment, mild cognitive impairment, glial activation, antioxidants, curcumin, quercetin, glial scar, calcium overload, PPARγ
- MeSH terms
- Alzheimer Disease, Animals, Antioxidants, Brain, Humans, Models, Neurological, Nerve Degeneration, Neuroglia, Drug Delivery Systems, Oxidative Stress, Inflammation Mediators
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