Cited by 427Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

Inflammatory process in Alzheimer's Disease

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Meraz-Ríos, Marco A., Toral-Rios, Danira, Franco-Bocanegra, Diana, Villeda-Hernández, Juana, Campos-Peña, Victoria·2013·Frontiers in Integrative Neuroscience

Abstract

Alzheimer Disease (AD) is a neurodegenerative disorder and the most common form of dementia. Histopathologically is characterized by the presence of two major hallmarks, the intracellular neurofibrillary tangles (NFTs) and extracellular neuritic plaques (NPs) surrounded by activated astrocytes and microglia. NFTs consist of paired helical filaments of truncated tau protein that is abnormally hyperphosphorylated. The main component in the NP is the amyloid-β peptide (Aβ), a small fragment of 40-42 amino acids with a molecular weight of 4 kD. It has been proposed that the amyloid aggregates and microglia activation are able to favor the neurodegenerative process observed in AD patients. However, the role of inflammation in AD is controversial, because in early stages the inflammation could have a beneficial role in the pathology, since it has been thought that the microglia and astrocytes activated could be involved in Aβ clearance. Nevertheless the chronic activation of the microglia has been related with an increase of Aβ and possibly with tau phosphorylation. Studies in AD brains have shown an upregulation of complement molecules, pro-inflammatory cytokines, acute phase reactants and other inflammatory mediators that could contribute with the neurodegenerative process. Clinical trials and animal models with non-steroidal anti-inflammatory drugs (NSAIDs) indicate that these drugs may decrease the risk of developing AD and apparently reduce Aβ deposition. Finally, further studies are needed to determine whether treatment with anti-inflammatory strategies, may decrease the neurodegenerative process that affects these patients.

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Crossref · 10.3389/fnint.2013.00059

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  • Activated microglia and reactive astrocytes produce nitric oxide and inflammatory cytokines such as IL-1, IL-6, TNF-α, and TGF-β, which contribute to a reinforced inflammatory cascade.

    “The activated microglia and reactive astrocytes produce nitric oxide (NO) and inflammatory cytokines, such as interleukin-1 (IL-1), IL-6, tumor necrosis factor α (TNF-α), and transforming growth factor β (TGF-β), that contribute to a reinforced inflammatory cascade [85, 97].”
  • The neuroinflammatory process in AD is mainly driven by innate immune cells in the brain, including microglia and astrocytes.

    “The neuroinflammatory process in AD is mainly driven by the innate immune cells in the brain, including microglia and astrocytes [85].”

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Authors
Meraz-Ríos, M. A., Toral-Rios, D., Franco-Bocanegra, D., Villeda-Hernández, J., & Campos-Peña, V.
Affiliations
Universidad Nacional Autónoma de México (MX)
Venue
Frontiers in Integrative Neuroscience
Published
2013
Volume
7
Pages
59-59
ISSN
1662-5145 (ISSN-L)
OpenAlex
W2142467924
Cited by
427
References
187
Citations by year
2026: 19 · 2025: 29 · 2024: 41 · 2023: 49 · 2022: 37 · 2021: 44 · 2020: 41 · 2019: 29 · 2018: 32 · 2017: 20 · 2016: 20 · 2015: 33 · 2014: 32 · 2013: 1
FWCI
19.91
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Frontiers in Integrative Neuroscience (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Consejo Nacional de Ciencia y Tecnología (157548)
  • Vlaamse regering
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
Alzheimer's disease, neuroinflammation, microglial activation, astrocytes, amyloid-beta, tau hyperphosphorylation, neurofibrillary tangles, neuritic plaques, complement system, inflammatory cytokines, acute phase proteins, nonsteroidal anti-inflammatory drugs, neurodegeneration, anti-inflammatory therapy

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