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Cited by 125Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

Neuroinflammatory Cytokines Induce Amyloid Beta Neurotoxicity through Modulating Amyloid Precursor Protein Levels/Metabolism

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Alasmari, Fawaz, Alshammari, Musaad A., Alasmari, Abdullah F., Alanazi, Wael A., Alhazzani, Khalid·2018·BioMed Research International
DOI 10.1155/2018/3087475PMC PMC6222241
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Abstract

Neuroinflammation has been observed in association with neurodegenerative diseases including Alzheimer’s disease (AD). In particular, a positive correlation has been documented between neuroinflammatory cytokine release and the progression of the AD, which suggests these cytokines are involved in AD pathophysiology. A histological hallmark of the AD is the presence of beta-amyloid (A β ) plaques and tau neurofibrillary tangles. Beta-amyloid is generated by the sequential cleavage of beta ( β ) and gamma ( γ ) sites in the amyloid precursor protein (APP) by β - and γ -secretase enzymes and its accumulation can result from either a decreased A β clearance or increased metabolism of APP. Previous studies reported that neuroinflammatory cytokines reduce the efflux transport of A β , leading to elevated A β concentrations in the brain. However, less is known about the effects of neuroinflammatory mediators on APP expression and metabolism. In this article, we review the modulatory role of neuroinflammatory cytokines on APP expression and metabolism, including their effects on β - and γ -secretase enzymes.

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  • Following infection, activated microglia and astrocytes secrete pro-inflammatory cytokines, including IL-1β, TNFα and IL-6, which are neurotoxic and may directly increase Aβ production via activation of β-secretase (BACE).

    “It has been shown that following infection, activated microglia and astrocytes secrete pro-inflammatory cytokines, including IL-1β, TNFα and IL-6 which are neurotoxic and may directly increase Aβ production via activation of β-secretase (BACE)66,74.”

    From Chlamydia pneumoniae can infect the central nervous system via the olfactory and trigeminal nerves and contributes to Alzheimer’s disease risk (2022) · cites this paper as [74]

    Section 2.2 reports that TNF-α and IFN-γ enhance β-secretase expression in an AD mouse model, with increased Aβ deposition. The Introduction also says inflammatory cytokines can cause neurodegeneration. Our copy does not establish the claimed sequence following infection or show that activated microglia and astrocytes secrete all three listed cytokines, including IL-6, to increase Aβ through β-secretase. Page numbers were not available in the indexed passages. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

  • Inflammatory proteins such as interleukin-1β, tumor necrosis factor-α, and interferon-γ can alter APP expression, APP processing, or Aβ transport.

    “Because inflammatory proteins (e.g., interleukin-1β, tumor necrosis factor–α, and interferon-γ) can alter APP expression, APP processing, or Aβ transport (47–50), the inflammatory changes caused by the deletion of Abi3 locus may have contributed to the increase in APP protein level and subsequently Aβ accumulation.”

    From Deletion of <i>Abi3</i> gene locus exacerbates neuropathological features of Alzheimer’s disease in a mouse model of Aβ amyloidosis (2021) · cites this paper as [50]

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Authors
Alasmari, F., Alshammari, M. A., Alasmari, A. F., Alanazi, W. A., & Alhazzani, K.
Affiliations
King Saud University (SA)
Corresponding author
Alasmari, Fawaz
ORCID
Venue
BioMed Research International
Publisher
Wiley
Published
2018-10-25
Volume
2018
Pages
1-8
ISSN
  • 1110-7243 (ISSN-L)
  • 2314-6133
  • 2314-6141
DOI
10.1155/2018/3087475
PMC
PMC6222241
OpenAlex
W2898432193
Cited by
125
References
87
Citations by year
2026: 13 · 2025: 15 · 2024: 11 · 2023: 15 · 2022: 20 · 2021: 21 · 2020: 24 · 2019: 6
FWCI
1.67
Type
journal article
Language
en
Open access
Licence
Locations
  • BioMed Research International (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
Deanship of Scientific Research and College of Pharmacy Research Center at King Saud University
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
neuroinflammatory cytokines, amyloid-beta, amyloid precursor protein, Alzheimer's disease, neuroinflammation, beta-secretase, gamma-secretase, APP metabolism, APP expression, neurotoxicity
MeSH terms
Alzheimer Disease, Animals, Brain, Disease Models, Animal, Humans, Cytokines, Amyloid beta-Peptides, Inflammation Mediators

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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