Abstract #3256

Glutamatergic dysfunction associated with tau depositions in Alzheimer’s disease

Kiwamu Matsuoka^1,2, Kosei Hirata¹, Naomi Kokubo¹, Kenji Tagai¹, Hironobu Endo¹, Keisuke Takahata¹, Hitoshi Shinotoh¹, Maiko Ono¹, Chie Seki¹, Kazunori Kawamura³, Ming-Rong Zhang³, Hitoshi Shimada^1,4, 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

Synopsis

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.

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