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Cited by 162Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsNeurological Disease Mechanisms and Treatments

The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.

Neuroimmunomodulation in the Pathogenesis of Alzheimer’s Disease

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Morales, Inelia, Farías, Gonzalo, Maccioni, Ricardo B.·2010·Neuroimmunomodulation
DOI 10.1159/000258724
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Abstract

Evidence has been cumulated on the role of microglia cells deregulation and alterations in their interaction patterns with brain neurons, in the pathway towards neurodegeneration in Alzheimer’s disease (AD). After the failure of the amyloid hypothesis to explain AD pathogenesis, current hypotheses focus on tau self-polymerization into pathological oligomers and filaments as a major culprit for neurofibrillary degeneration. It is worth pointing out that formation of tau polymers is consistent with the clinical and neuropathological observations, and that tangles are pathognomonic of AD and related tau disorders. In this context, inflammatory processes play a major role in neuronal degeneration. On the basis of studies on microglia and neuronal cultures, together with experiments in animal models, and the clinical evidence, we postulated that a series of endogenous damage signals activate microglia cells, inducing NFĸ-β with the consequent release of cytokine mediators such as TNF-α, IL-6 and IL-1β. An overexpression of these mediators may trigger signaling cascades in neurons leading to activation of protein kinases gsk3β, cdk5, abl kinases, along with inactivation of phosphatases such as PP1, with the resulting hyperphosphorylation and self-aggregation of tau protein into neurotoxic oligomeric species.

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  1. 10.1016%2Fj.arcmed.2007.10.001 · DOI · Paper page

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Metadata

Authors
Morales, I., Farías, G., & Maccioni, R. B.
Affiliations
University of Chile (CL)
ORCID
Maccioni, Ricardo B.
Venue
Neuroimmunomodulation
Publisher
S. Karger AG
Published
2010
Volume
17
Issue
3
Pages
202-204
ISSN
  • 1021-7401 (ISSN-L)
  • 1423-0216
DOI
10.1159/000258724
OpenAlex
W2047052426
Cited by
162
References
9
Citations by year
2026: 2 · 2025: 7 · 2024: 5 · 2023: 11 · 2022: 9 · 2021: 10 · 2020: 6 · 2019: 7 · 2018: 12 · 2017: 6 · 2016: 12 · 2015: 12 · 2014: 12 · 2013: 20 · 2012: 16
FWCI
10.83
Type
journal article
Language
en
Open access
Licence
Locations
  • NeuroImmunoModulation (publishedVersion)
  • PubMed (publishedVersion)
  • Americanae (AECID Library) (submittedVersion, other-oa)
  • LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, other-oa)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords
Alzheimer's disease, microglia, neuroinflammation, tau hyperphosphorylation, tau oligomers, neurofibrillary tangles, NF-κB signaling, TNF-α, interleukin-6, IL-1β, GSK3β, cyclin-dependent kinase 5, c-Abl, PP1 phosphatase, neurodegeneration, amyloid hypothesis
MeSH terms
Alzheimer Disease, Animals, Encephalitis, Gliosis, Humans, Nerve Degeneration, Neuroimmunomodulation, Signal Transduction, Cytokines, Microglia, Toll-Like Receptor 4

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