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Peer-reviewedCC BYFrontiers in aging neuroscience

Sex and stage-defined exploratory inflammatory and amyloid-associated readout patterns in female APP/PS1 mice exposed to TAK-242.

  • Xiaolu Ren1,2
  • Ting Li1
  • Shan Liu1
  • Ling Li3
  • Fang Li4
4 affiliations
  1. 1Department of Radiology, General Hospital of Ningxia Medical University, Yinchuan, Ningxia, China.
  2. 2School of Health Sciences, Universiti Sains Malaysia, Kubang Kerian, Kelantan, Malaysia.
  3. 3Department of Hematology, General Hospital of Ningxia Medical University, Yinchuan, Ningxia, China.
  4. 4Department of Neurology, General Hospital of Ningxia Medical University, Yinchuan, Ningxia, China.
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Abstract

TLR4-related inflammatory signaling has been implicated in Alzheimer's disease-related immune responses, and TAK-242 has been used as an experimental tool in studies examining this signaling context. This exploratory study characterized inflammatory cytokine and amyloid-associated histological readout patterns associated with TAK-242 exposure in female early-stage APP/PS1 mice. Female APP/PS1 mice were assigned to saline, lipopolysaccharide, or TAK-242 exposure conditions for 6 weeks, with age-matched non-transgenic mice serving as reference controls (n = 8/group). Brain TNF-α, IL-1β, and IL-6 levels were measured by ELISA, and 6E10-positive staining area was quantified by immunohistochemistry. Directional differences in cytokine levels and 6E10-positive staining area were observed between APP/PS1 mice exposed to TAK-242 and untreated APP/PS1 mice. However, because a vehicle-matched APP/PS1 control group was not included, these differences cannot be attributed specifically to TAK-242 and were interpreted as exploratory exposure-associated patterns rather than pharmacological efficacy. This study provides a sex and stage-defined exploratory dataset of inflammatory and amyloid-associated readout patterns in female early-stage APP/PS1 mice to inform future vehicle-controlled investigations.

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Cite

BibTeXRIS
BibTeX
@article{ren2026stagedefined,
  title = {{Sex and stage-defined exploratory inflammatory and amyloid-associated readout patterns in female APP/PS1 mice exposed to TAK-242.}},
  author = {Xiaolu Ren and Ting Li and Shan Liu and Ling Li and Fang Li},
  journal = {Frontiers in aging neuroscience},
  year = {2026},
  month = oct,
  doi = {10.3389/fnagi.2026.1944097},
  url = {https://europepmc.org/article/MED/42952777},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Sex and stage-defined exploratory inflammatory and amyloid-associated readout patterns in female APP/PS1 mice exposed to TAK-242.
AU  - Xiaolu Ren
AU  - Ting Li
AU  - Shan Liu
AU  - Ling Li
AU  - Fang Li
PY  - 2026
DA  - 2026/10/14
JO  - Frontiers in aging neuroscience
DO  - 10.3389/fnagi.2026.1944097
UR  - https://europepmc.org/article/MED/42952777
AB  - TLR4-related inflammatory signaling has been implicated in Alzheimer's disease-related immune responses, and TAK-242 has been used as an experimental tool in studies examining this signaling context. This exploratory study characterized inflammatory cytokine and amyloid-associated histological readout patterns associated with TAK-242 exposure in female early-stage APP/PS1 mice. Female APP/PS1 mice were assigned to saline, lipopolysaccharide, or TAK-242 exposure conditions for 6 weeks, with age-matched non-transgenic mice serving as reference controls (n = 8/group). Brain TNF-α, IL-1β, and IL-6 levels were measured by ELISA, and 6E10-positive staining area was quantified by immunohistochemistry. Directional differences in cytokine levels and 6E10-positive staining area were observed between APP/PS1 mice exposed to TAK-242 and untreated APP/PS1 mice. However, because a vehicle-matched APP/PS1 control group was not included, these differences cannot be attributed specifically to TAK-242 and were interpreted as exploratory exposure-associated patterns rather than pharmacological efficacy. This study provides a sex and stage-defined exploratory dataset of inflammatory and amyloid-associated readout patterns in female early-stage APP/PS1 mice to inform future vehicle-controlled investigations.
SN  - 1663-4365
ER  -