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
Open accessAbstract
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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“This results in tau phosphorylation and formation of neurotoxic oligomers and fibrils, further amplifying glial activation and brain inflammation. 99”
From Senescence, brain inflammation, and oligomeric tau drive cognitive decline in Alzheimer's disease: Evidence from clinical and preclinical studies (2024) · cites this paper as [99]
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Cites
McGeer, P. L., Schulzer, M., & McGeer, E. G. (1996) · Neurology · doi:10.1212/wnl.47.2.425 · Cited by 1,367
Quintanilla, R. A., Orellana, D. I., González-Billault, C., & Maccioni, R. B. (2004) · Experimental Cell Research · doi:10.1016/j.yexcr.2004.01.002 · Cited by 455
Self-citationBattista, D., Ferrari, C. C., Gage, F. H., & Pitossi, F. J. (2006) · European Journal of Neuroscience · doi:10.1111/j.1460-9568.2005.04539.x · Cited by 306
The Role of Neuroimmunomodulation in Alzheimer's Disease
Maccioni, R. B., Rojo, L. E., Fernández, J. A., & Kuljiš, R. O. (2009) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2008.03972.x · Cited by 261
Self-citationNatural variation and genetic covariance in adult hippocampal neurogenesis
Kempermann, G., Chesler, E. J., Lu, L., Williams, R. W., & Gage, F. H. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0510291103 · Cited by 202
TLR Activation Induces TNF-α Production from Adult Neural Stem/Progenitor Cells
Covacu, R., Arvidsson, L., Andersson, Å., Khademi, M., Erlandsson-Harris, H., Harris, R. A., Svensson, M. A., Olsson, T. P., & Brundin, L. (2009) · The Journal of Immunology · doi:10.4049/jimmunol.0802907 · Cited by 78
The Damage Signals Hypothesis of Alzheimer's Disease Pathogenesis
Fernández, J. A., Rojo, L. E., Kuljiš, R. O., & Maccioni, R. B. (2008) · Journal of Alzheimer s Disease · doi:10.3233/jad-2008-14307 · Cited by 77
Self-citationMild Cognitive Impairment and Alzheimer Patients Display Different Levels of Redox-Active CSF Iron
Manuel Lavados, M., Guillón, M., Mujica, M. C., Rojo, L. E., Fuentes, P., & Maccioni, R. B. (2008) · Journal of Alzheimer s Disease · doi:10.3233/jad-2008-13211 · Cited by 61
Self-citationNeuroprotective effect of TNFα against the β-amyloid neurotoxicity mediated by CDK5 kinase
Orellana, D. I., Quintanilla, R. A., & Maccioni, R. B. (2006) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2006.10.010 · Cited by 36
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- 10.1016%2Fj.arcmed.2007.10.001 · DOI · Paper page
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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-citationMorales, I., Guzmán-MartÃnez, L., Cerda-Troncoso, C., FarÃas, G. A., & Maccioni, R. B. (2014) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2014.00112 · Cited by 490
Self-citationBrain metabolic dysfunction at the core of Alzheimer's disease
de la Monte, S. M., & Tong, M. (2014) · Biochemical Pharmacology · doi:10.1016/j.bcp.2013.12.012 · Cited by 472
Brain Insulin Resistance and Deficiency as Therapeutic Targets in Alzheimers Disease
de la Monte, S. M. (2012) · Current Alzheimer Research · doi:10.2174/156720512799015037 · Cited by 468
Alzheimer’s Disease: An Updated Overview of Its Genetics
Andrade-Guerrero, J., Santiago-Balmaseda, A., Jeronimo-Aguilar, P., Vargas-Rodríguez, I., Cadena-Suárez, A. R., Sánchez-Garibay, C., Pozo-Molina, G., Méndez-Catalá, C. F., Cardenas-Aguayo, M.-D.-C., Diaz-Cintra, S., et al. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24043754 · Cited by 336
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
- 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
- green
- americanae.aecid.es
- 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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