Neuroimmunomodulation in the Pathogenesis of Alzheimer’s Disease
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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.
“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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Self-citationVitamin D Insufficiency in Psychiatric Inpatients
Rylander, M., & Verhulst, S. J. (2013) · Journal of Psychiatric Practice · doi:10.1097/01.pra.0000432599.24761.c1 · Cited by 26 · see citing works
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- 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
- Health Sciences › Medicine › Physiology › 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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