Cited by 685Neuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsNeurological Disease Mechanisms and Treatments

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Neuroinflammation, Oxidative Stress and the Pathogenesis of Alzheimers Disease

Agostinho, Paula, A. Cunha, Rodrigo, Oliveira, Catarina·2010·Current Pharmaceutical Design

DOI 10.2174/138161210793176572

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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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Authors: Agostinho, P., A. Cunha, R., & Oliveira, C.
Affiliations: University of Coimbra (PT)
Corresponding author: Oliveira, Catarina
ORCID: Agostinho, Paula
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)
DOI: 10.2174/138161210793176572
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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Neuroinflammation, Oxidative Stress and the Pathogenesis of Alzheimers Disease

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