Long-Term Pioglitazone Treatment Has No Significant Impact on Microglial Activation and Tau Pathology in P301S Mice

Lea Helena Kunze; François Ruch; Gloria Biechele; Florian Eckenweber; Karin Wind-Mark; Lina Dinkel; Paul Feyen; Peter Bartenstein; Sibylle Ziegler; Lars Paeger; Sabina Tahirovic; Jochen Herms; Matthias Brendel

doi:10.20944/preprints202304.1153.v1

Preprint Communication Version 1 Preserved in Portico This version is not peer-reviewed

Version 1 : Received: 28 April 2023 / Approved: 28 April 2023 / Online: 28 April 2023 (08:56:28 CEST)

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 the last years, the peroxisome proliferator-activated receptor γ (PPARγ) 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-β (Aβ) 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 Aβ-dependent microglial activation, but does not significantly modulate microglial activation in response to tau pathology.

microglia; pioglitazone; TSPO-PET

Medicine and Pharmacology, Neuroscience and Neurology

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Long-Term Pioglitazone Treatment Has No Significant Impact on Microglial Activation and Tau Pathology in P301S Mice

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