Neuroinflammation in the pathogenesis of Alzheimer’s disease. A rational framework for the search of novel therapeutic approaches
Open accessAbstract
Alzheimer disease (AD) is the most common cause of dementia in people over 60 years old. The molecular and cellular alterations that trigger this disease are still diffuse, one of the reasons for the delay in finding an effective treatment. In the search for new targets to search for novel therapeutic avenues, clinical studies in patients who used anti-inflammatory drugs indicating a lower incidence of AD have been of value to support the neuroinflammatory hypothesis of the neurodegenerative processes and the role of innate immunity in this disease. Neuroinflammation appears to occur as a consequence of a series of damage signals, including trauma, infection, oxidative agents, redox iron, oligomers of τ and β-amyloid, etc. In this context, our theory of Neuroimmunomodulation focus on the link between neuronal damage and brain inflammatory process, mediated by the progressive activation of astrocytes and microglial cells with the consequent overproduction of proinflammatory agents. Here, we discuss about the role of microglial and astrocytic cells, the principal agents in neuroinflammation process, in the development of neurodegenerative diseases such as AD. In this context, we also evaluated the potential relevance of natural anti-inflammatory components, which include curcumin and the novel Andean Compound, as agents for AD prevention and as a coadjuvant for AD treatments.
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It remains unclear whether microglial activation is a primary triggering mechanism or merely a consequence of protein aggregate accumulation.
“it remains unclear whether microglial activation is a primary triggering mechanism or merely a consequence of protein aggregate accumulation [60]”
From Theranostic Nanoplatforms for Alzheimer's Disease: A Critical Analysis of Conceptual Contradictions (2026) · cites this paper as [60]
The Microglial cell section (page unavailable) describes a feedback loop: tau aggregates activate microglia, while activated microglia contribute to neuronal death and further aggregate release. This supports a complex relationship, but the paper does not explicitly say that which process comes first remains unclear, and it does not characterize microglial activation as merely a consequence of aggregate accumulation. (LLM, conf=0.82)
Experimental — accuracy not yet measuredIn Alzheimer's disease, neuroinflammation is primarily thought to be a consequence of a series of damage signals including trauma, oxidation, oligomers of Aβ and tau, and more.
“In Alzheimer’s disease, neuroinflammation is primarily thought to be a consequence of a series of damage signals including trauma, oxidation, oligomers of Aβ and tau, and more [67].”
From Age, sex and Alzheimer’s disease: a longitudinal study of 3xTg-AD mice reveals sex-specific disease trajectories and inflammatory responses mirrored in postmortem brains from Alzheimer’s patients (2024) · cites this paper as [67]
The Neuroinflammation section describes inflammation as generally secondary to an initial event such as trauma, and the Microglial cell section says Aβ protofibrils and pathological tau aggregates can activate microglia. The paper does not clearly identify oxidation as an initiating damage signal; its Neuroinflammation table instead lists oxidative stress as an effect of inflammatory products. No page numbers are available in our copy. (LLM, conf=0.85)
Experimental — accuracy not yet measuredPro-inflammatory cytokines and chemokines secreted into the immediate neurological environment accelerate neuronal injury and eventually neuron death.
“Pro-inflammatory cytokines and chemokines secreted into the immediate neurological environment accelerate neuronal injury and eventually neuron death (Aktas et al., 2007; Heckmann et al., 2018; Morales et al.,2014).”
From LC3-Associated Endocytosis Facilitates β-Amyloid Clearance and Mitigates Neurodegeneration in Murine Alzheimer’s Disease (2019) · cites this paper as Morales et al.,2014
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“Neuroinflammation, the inflammation of the central nervous system (CNS), is considered as a fundamental process of many pathologic conditions in the brain, such as Alzheimer’s disease and major depressive disorder (Hurley and Tizabi, 2013; Morales et al., 2014).”
BackgroundNeuroinflammation in Alzheimer’s disease: Pleiotropic roles for cytokines and neuronal pentraxins
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- Authors
- Morales, I., Guzmán-MartÃnez, L., Cerda-Troncoso, C., FarÃas, G. A., & Maccioni, R. B.
- Affiliations
- University of Chile (CL)
- Corresponding author
- Maccioni, Ricardo B.
- ORCID
- Maccioni, Ricardo B.
- Venue
- Frontiers in Cellular Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2014-04-22
- Volume
- 8
- Pages
- 112-112
- ISSN
- 1662-5102 (ISSN-L)
- PMC
- PMC4001039
- OpenAlex
- W2109984042
- Cited by
- 490
- References
- 85
- Citations by year
- 2026: 13 · 2025: 26 · 2024: 43 · 2023: 38 · 2022: 45 · 2021: 40 · 2020: 50 · 2019: 48 · 2018: 45 · 2017: 50 · 2016: 25 · 2015: 50 · 2014: 14 · 2012: 1
- FWCI
- 3.75
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Cellular Neuroscience (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Americanae (AECID Library) (publishedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, other-oa)
- Universidad de Chile (submittedVersion, cc-by-nc-nd)
- Funders
- Corporación de Fomento de la Producción
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- Alzheimer's disease, neuroinflammation, neuroimmunomodulation, microglia, astrocytes, innate immunity, anti-inflammatory agents, tau oligomers, amyloid-beta, oxidative stress, iron, curcumin, neurodegeneration, therapeutic target
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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