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Updated: Aug 7, 2026

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Assessment of Spontaneous Alternation, Novel Object Recognition and Limb Clasping in Transgenic Mouse Models of Amyloid-β and Tau Neuropathology
Published on: May 28, 2017
CXCL10 contributes to female-specific pathological progression in tauopathy model mice
Ryohei Uenishi1, Rinna Kawata1,2, Tatsuya Manabe1,2
1Department of Neurocognitive Science, Institute of Brain Science, Graduate School of Medical Sciences, Nagoya City University, Nagoya, 467-8601, Japan.
Journal of Neuroinflammation
|August 6, 2026
Summary
The study identifies C-X-C motif chemokine ligand 10 (CXCL10) as a key driver of tauopathy progression. Targeting CXCL10 shows potential for treating tau pathology, particularly in female mice.
Area of Science:
- Neuroscience
- Immunology
- Genetics
Background:
- Neuroinflammation is crucial in tauopathy progression.
- The molecular links between neuroinflammation and tau pathology are not fully understood.
Purpose of the Study:
- To identify key inflammatory mediators linking glial activation and T cell accumulation to tau pathology.
- To investigate the role of C-X-C motif chemokine ligand 10 (CXCL10) in tauopathy.
Main Methods:
- Utilized P301S-mutant tau transgenic mice.
- Employed spatial transcriptomics to identify CXCL10 expression patterns.
- Used genetic ablation of Cxcl10 to assess its impact on tau pathology and survival.
Main Results:
- CXCL10 is upregulated in tauopathy brains, mainly expressed by astrocytes.
- Genetic ablation of Cxcl10 attenuated tau accumulation and prolonged survival in female mice.
- CXCL10 deficiency reduced T cell infiltration but did not alter neurodegeneration or motor deficits.
Conclusions:
- CXCL10 is a critical inflammatory mediator in sex-specific tau-associated pathology.
- CXCL10 contributes to tau pathology through multiple inflammatory pathways.
- Further research is needed to elucidate the sex-dependent mechanisms of CXCL10 in tauopathy.

