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Cited by 504Neuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsNeurological Disease Mechanisms and Treatments

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

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Morales, Inelia, Guzmán-Martínez, Leonardo, Cerda-Troncoso, Cristóbal, Farías, Gonzalo A., Maccioni, Ricardo B.·2014·Frontiers in Cellular Neuroscience
DOI 10.3389/fncel.2014.00112PMC PMC4001039
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Abstract

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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Crossref · 10.3389/fncel.2014.00112

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Figure 1 The neuroinflammatory process. By sensing signals of damage or injury, astrocytes and microglia suffer a gradual activation process, leading to morphological changes and secretion of pro-inflammatory elements (i.e., cytokines, cytotoxic elements, ROS). Thus, the constant exposure of astrocytes and microglia to factor causing injuries and secretion of these elements induce mutual activation of microglial cells and astrocytes, along with neuroinflammatory process that eventually trigger neuronal death.
Figure 1 The neuroinflammatory process. By sensing signals of damage or injury, astrocytes and microglia suffer a gradual activation process, leading to morphological changes and secretion of pro-inflammatory elements (i.e., cytokines, cytotoxic elements, ROS). Thus, the constant exposure of astrocytes and microglia to factor causing injuries and secretion of these elements induce mutual activation of microglial cells and astrocytes, along with neuroinflammatory process that eventually trigger neuronal death.CC BY · PubMed Central
Figure 2 τ aggregates potentiate the neuroinflammatory process. Activated microglia and astrocytes, induce neuronal death through neuroinflammatory process, allowing the release of τ protein aggregates from the dead neuron. These aggregates of τ are capable of inducing activation of microglia and astrocytes, as well as neuronal death, thus producing a circuit of constant neuroinflammation. Considering the possible protective effects of curcumin, neuronal death could be delayed or inhibited by this compound, halting this circuit of neuroinflammation. Furthermore, the nutraceutical complex Brain Up-10 acts on τ aggregates, and may prevent neuronal death and activation of microglia and astrocytes, stopping the circuit and the development of neuroinflammation.
Figure 2 τ aggregates potentiate the neuroinflammatory process. Activated microglia and astrocytes, induce neuronal death through neuroinflammatory process, allowing the release of τ protein aggregates from the dead neuron. These aggregates of τ are capable of inducing activation of microglia and astrocytes, as well as neuronal death, thus producing a circuit of constant neuroinflammation. Considering the possible protective effects of curcumin, neuronal death could be delayed or inhibited by this compound, halting this circuit of neuroinflammation. Furthermore, the nutraceutical complex Brain Up-10 acts on τ aggregates, and may prevent neuronal death and activation of microglia and astrocytes, stopping the circuit and the development of neuroinflammation.CC BY · PubMed Central

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Research works printed but not linked: 1

  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

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Metadata

Authors
Morales, I., Guzmán-Martínez, L., Cerda-Troncoso, C., Farías, 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)
DOI
10.3389/fncel.2014.00112
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
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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