Affiliations: [a] National Institutes for Quantum and Radiological Science and Technology, Chiba, Japan
| [b] Department of Neurology, Graduate School of Medicine, Chiba University, Chiba, Japan
Correspondence:
[*]
Correspondence to: Naruhiko Sahara, Department of Functional Brain Imaging Research,
National Institute of Radiological Sciences,
National Institutes for Quantum and Radiological Science and Technology,
Chiba 263-8555, Japan. Tel.: +81 43 206 3251; Fax: +81 43 253 0396;
E-mail: [email protected].
Abstract: Tauopathy is characterized by the fibrillar tau accumulation in neurons and glial cells. In order to advance our understanding of the causative mechanisms of tauopathy, neuroinflammation, which has been suggested to play important roles in disease progression, will require particular attention. Neuroinflammation is characterized predominantly by microglial activation. At present, it is still under debate whether microglial activation is a cause or a result of neurodegeneration. To search for a temporal relationship between neurodegeneration and neuroinflammation, our group demonstrated that in vivo imaging (e.g., tau-PET, TSPO-PET, and volumetric MRI) of tauopathy mice strongly supports the evidence of microglial activation along with both pathological tau accumulation and brain atrophy. Both in vivo imaging and histochemical analysis confirmed that microglial TSPO accumulation was the late event during the pathogenesis of tauopathy. On the other hand, it is known that purinergic receptor P2Y12 as a marker of homeostatic microglia cells was reduced at an early stage of disease progression. In this review, we will introduce a phenotypic change of microglia in a mouse model of tauopathy and propose novel approaches to the establishment of imaging biomarkers, thereby targeting the early diagnosis of tauopathy.
Keywords: Microglia, neuroinflammation, P2Y12 receptor, PET imaging, tauopathy, TSPO
