Glutamatergic dysfunction associated with tau depositions in Alzheimer’s disease
Kiwamu Matsuoka1,2, Kosei Hirata1, Naomi Kokubo1, Kenji Tagai1, Hironobu Endo1, Keisuke Takahata1, Hitoshi Shinotoh1, Maiko Ono1, Chie Seki1, Kazunori Kawamura3, Ming-Rong Zhang3, Hitoshi Shimada1,4, Yuhei Takado1, and Makoto Higuchi1
1Department of Functional Brain Imaging, Institute for Quantum Medical Science, Quantum Life and Medical Science Directorate, National Institutes for Quantum Science and Technology, Chiba-shi, Japan, 2Department of Psychiatry, Nara Medical University, Kashihara-shi, Japan, 3Department of Advanced Nuclear Medicine Sciences, Institute for Quantum Medical Science, Quantum Life and Medical Science Directorate, National Institutes for Quantum Science and Technology, Chiba-shi, Japan, 4Department of Functional Neurology & Neurosurgery, Center for Integrated Human Brain Science, Brain Research Institute, Niigata University, Niigata-shi, Japan
Glutamatergic neurons and cingulate cortices have crucial roles in the cognitive dysfunction of Alzheimer's disease (AD). This study aimed to evaluate regional vulnerabilities of the glutamatergic system in AD at the level of the cingulate gyrus in relation to tau and amyloid-β (Aβ) depositions. Combining MRSI and PET, we found that the glutamatergic system in the posterior cingulate cortex (PCC) is vulnerable to tau deposits but not Aβ from the early stage of AD, and glutamate in the PCC region may be a marker of disease progression in AD.
This abstract and the presentation materials are available to members only;
a login is required.