| First Author | Kunze LH | Year | 2023 |
| Journal | Int J Mol Sci | Volume | 24 |
| Issue | 12 | PubMed ID | 37373253 |
| Mgi Jnum | J:337435 | Mgi Id | MGI:7495046 |
| Doi | 10.3390/ijms241210106 | Citation | Kunze LH, et al. (2023) Long-Term Pioglitazone Treatment Has No Significant Impact on Microglial Activation and Tau Pathology in P301S Mice. Int J Mol Sci 24(12) |
| abstractText | Neuroinflammation is one disease hallmark on the road to neurodegeneration in primary tauopathies. Thus, immunomodulation might be a suitable treatment strategy to delay or even prevent the occurrence of symptoms and thus relieve the burden for patients and caregivers. In recent years, the peroxisome proliferator-activated receptor gamma (PPARgamma) has received increasing attention as it is immediately involved in the regulation of the immune system and can be targeted by the anti-diabetic drug pioglitazone. Previous studies have shown significant immunomodulation in amyloid-beta (Abeta) mouse models by pioglitazone. In this study, we performed long-term treatment over six months in P301S mice as a tauopathy model with either pioglitazone or placebo. We performed serial 18 kDa translocator protein positron-emission-tomography (TSPO-PET) imaging and terminal immunohistochemistry to assess microglial activation during treatment. Tau pathology was quantified via immunohistochemistry at the end of the study. Long-term pioglitazone treatment had no significant effect on TSPO-PET, immunohistochemistry read-outs of microglial activation, or tau pathology levels in P301S mice. Thus, we conclude that pioglitazone modifies the time course of Abeta-dependent microglial activation, but does not significantly modulate microglial activation in response to tau pathology. |
