Cited by 29Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

IL-3 Control Tau Modifications and Protects Cortical Neurons from Neurodegeneration

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Zambrano, A., Otth, C., B. Maccioni, R., I. Concha, I.·2010·Current Alzheimer Research

Abstract

Interleukin-3 (IL-3) regulates the proliferation, survival and differentiation of haematopoietic cells via interaction with specific cell-surface receptors. IL-3 is expressed in several non-hematopoietic cell types. Studies have demonstrated the presence of IL-3 in the central nervous system, however, its physiological role in these cells is poorly understood. Previously we have been demonstrated that IL-3 prevents neuronal death induced by fibrillary β amyloid in these cells, by PI 3-kinase and Jak/STAT pathway activation. In this study, we demonstrated that IL-3 significantly reduced Aβ-promoted neurite degeneration and toxicity. Thus, this cytokine provides cellular protection against Aβ neurotoxicity in primary cortical neuronal cells, by modulating microtubular dynamics and prevention of tau cleavage and hyperphosphorylation. We also demonstrates that IL-3 is expressed in the "in vivo" mouse model of AD, Tg2576, which also expresses human AβPP with the Swedish mutation. In summary, these results suggest that IL-3 could play a neuroprotective role in AD.

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Crossref · 10.2174/156720510793499011

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  • Other inflammatory factors such as IL-3, IL-6, IL-18, TNFα, and MIF are involved in tau phosphorylation and/or truncation.

    “Other inflammatory factors such as IL-3, IL-6, IL-18, tumor necrosis factor-α (TNFα), and macrophage migration inhibitory factor (MIF) are also found to be involved in tau phosphorylation and/or truncation [166–170].”

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Authors
Zambrano, A., Otth, C., B. Maccioni, R., & I. Concha, I.
Venue
Current Alzheimer Research
Published
2010-11-01
Volume
7
Issue
7
Pages
615-624
ISSN
1567-2050 (ISSN-L)
OpenAlex
W1967250452
Cited by
29
References
0
Citations by year
2026: 2 · 2025: 4 · 2024: 4 · 2023: 3 · 2022: 2 · 2021: 2 · 2019: 1 · 2018: 1 · 2017: 2 · 2016: 3 · 2015: 1 · 2014: 1 · 2013: 2 · 2012: 1
FWCI
0.64
Type
journal article
Language
en
Open access
Licence
other-oa
Locations
  • Current Alzheimer Research (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
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
interleukin-3, tau hyperphosphorylation, tau cleavage, amyloid-beta toxicity, cortical neurons, neuroprotection, Alzheimer's disease, neurite degeneration, microtubule dynamics, PI3K signaling, JAK/STAT signaling, Tg2576 mice, neurodegeneration
MeSH terms
Alzheimer Disease, Animals, Cells, Cultured, Humans, Interleukin-3, Mice, Inbred C57BL, Mice, Transgenic, Nerve Degeneration, Amyloid beta-Peptides, tau Proteins, Cytoprotection, Mice

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