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Cited by 206Neuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsDementia and Cognitive Impairment Research

Inflammation context in Alzheimer’s disease, a relationship intricate to define

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Novoa, Catalina, Salazar, Paulina, Cisternas, Pedro, Gherardelli, Camila, Vera-Salazar, Roberto, Zolezzi, Juan M., Inestrosa, Nibaldo C.·2022·Biological Research
DOI 10.1186/s40659-022-00404-3PMC PMC9784299
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Abstract

Alzheimer’s disease (AD), the most common form of dementia, is characterized by the accumulation of amyloid β (Aβ) and hyperphosphorylated tau protein aggregates. Importantly, Aβ and tau species are able to activate astrocytes and microglia, which release several proinflammatory cytokines, such as tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β), together with reactive oxygen (ROS) and nitrogen species (RNS), triggering neuroinflammation. However, this inflammatory response has a dual function: it can play a protective role by increasing Aβ degradation and clearance, but it can also contribute to Aβ and tau overproduction and induce neurodegeneration and synaptic loss. Due to the significant role of inflammation in the pathogenesis of AD, several inflammatory mediators have been proposed as AD markers, such as TNF-α, IL-1β, Iba-1, GFAP, NF-κB, TLR2, and MHCII. Importantly, the use of anti-inflammatory drugs such as NSAIDs has emerged as a potential treatment against AD. Moreover, diseases related to systemic or local inflammation, including infections, cerebrovascular accidents, and obesity, have been proposed as risk factors for the development of AD. In the following review, we focus on key inflammatory processes associated with AD pathogenesis.

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  • Proinflammatory cytokines enhance tau phosphorylation through kinase activation pathways involving CDK5, GSK-3, and MAPKs, thereby accelerating neurofibrillary tangle formation.

    “Proinflammatory cytokines enhance tau phosphorylation through kinase activation pathways involving CDK5, GSK-3, and MAPKs, thereby accelerating neurofibrillary tangle formation [92] (Fig. 6).”

    From Toward a Unified Framework in Molecular Neurobiology of Alzheimer’s Disease: Revisiting the Pathophysiological Hypotheses (2026) · cites this paper as [92]

    The “Neuroinflammation related to tau” section (page unavailable) says neuroinflammation could play a role in tau hyperphosphorylation and neurofibrillary tangle formation. It does not establish the claimed CDK5/GSK-3/MAPK pathway or accelerated tangle formation; its p38 MAPK passage instead describes extracellular tau activating a pathway in microglia that increases cytokine expression. (LLM, conf=0.88)

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Cited by

Sorted by citations

Authors
Novoa, C., Salazar, P., Cisternas, P., Gherardelli, C., Vera-Salazar, R., Zolezzi, J. M., & Inestrosa, N. C.
Affiliations
  • Pontificia Universidad Católica de Chile (CL)
  • University of O'Higgins (CL)
  • Universidad de Santiago de Chile (CL)
  • Universidad de Magallanes (CL)
Corresponding author
Inestrosa, Nibaldo C.
ORCID
Venue
Biological Research
Publisher
Springer Science and Business Media LLC
Published
2022-12-23
Volume
55
Issue
1
Pages
39-39
ISSN
  • 0716-9760 (ISSN-L)
  • 0717-6287
DOI
10.1186/s40659-022-00404-3
PMC
PMC9784299
OpenAlex
W4312178155
Cited by
206
References
44
Citations by year
2026: 54 · 2025: 75 · 2024: 55 · 2023: 22
FWCI
3.88
Type
journal article
Language
en
Open access
Licence
Locations
  • Biological Research (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
FONIS (EULACH16/T010131, EULACH16/T010132)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
Alzheimer's disease, neuroinflammation, amyloid-beta, tau hyperphosphorylation, astrocytes, microglia, inflammatory cytokines, TNF-α, IL-1β, reactive oxygen species, reactive nitrogen species, neurodegeneration, synaptic loss, anti-inflammatory agents, nonsteroidal anti-inflammatory drugs, NF-κB, TLR2, MHC class II, Iba1, glial fibrillary acidic protein, dementia risk factors, infection, cerebrovascular disease, obesity
MeSH terms
Alzheimer Disease, Humans, Inflammation, Tumor Necrosis Factor-alpha, Amyloid beta-Peptides, NF-kappa B, Microglia

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