The DOI matches its Crossref record; 85 of the 85 references it cites were found in a registry or an index.
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 [60]”
From Theranostic Nanoplatforms for Alzheimer's Disease: A Critical Analysis of Conceptual Contradictions (2026) · cites this paper as [60]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“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]
Experimental — accuracy not yet measuredIn the citing paper
“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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Cites
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Background
Research works printed but not linked: 1
- Powell, 1999, Dissection of astrocyte-mediated cues in neuronal guidance and process extension, Glia, 26, 73, 10.1002/(sici)1098-1136(199903)26:173::aid-glia83.0.co;2-s · DOI
Cited by
Sorted by citations
Neuroinflammation in Alzheimer's disease: current evidence and future directions
Calsolaro, V., & Edison, P. (2016) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2016.02.010 · Cited by 1,726
Microglia in Neurological Diseases: A Road Map to Brain-Disease Dependent-Inflammatory Response
Bachiller, S., Jiménez-Ferrer, I., Paulus, A., Yang, Y., Swanberg, M., Deierborg, T., & Boza‐Serrano, A. (2018) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2018.00488 · Cited by 750
Neuroinflammation as a common feature of neurodegenerative disorders
Guzman-Martinez, L., Maccioni, R. B., Andrade, V., Navarrete, L. P., Pastor, M. G., & Ramos-Escobar, N. (2019) · Frontiers in Pharmacology · doi:10.3389/fphar.2019.01008 · Cited by 702
Self-citationDrug treatments in Alzheimer’s disease
Briggs, R., Kennelly, S. P., & O’Neill, D. (2016) · Clinical Medicine · doi:10.7861/clinmedicine.16-3-247 · Cited by 571
Inflammatory Response in the CNS: Friend or Foe?
Sochocka, M., Diniz, B. S., & Leszek, J. (2017) · Molecular Neurobiology · doi:10.1007/s12035-016-0297-1 · Cited by 573
Metadata
- 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
- 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
- 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, neuroimmunomodulation, microglia, astrocytes, innate immunity, anti-inflammatory agents, tau oligomers, amyloid-beta, oxidative stress, iron, curcumin, neurodegeneration, therapeutic target
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