Fluorine-19 Magnetic Resonance Imaging for Detection of Amyloid β Oligomers Using a Keto Form of Curcumin Derivative in a Mouse Model of Alzheimer's Disease.
Daijiro YanagisawaNor Faeizah IbrahimHiroyasu TaguchiShigehiro MorikawaTakami TomiyamaIkuo TooyamaPublished in: Molecules (Basel, Switzerland) (2021)
Recent evidence suggests that the formation of soluble amyloid β (Aβ) aggregates with high toxicity, such as oligomers and protofibrils, is a key event that causes Alzheimer's disease (AD). However, understanding the pathophysiological role of such soluble Aβ aggregates in the brain in vivo could be difficult due to the lack of a clinically available method to detect, visualize, and quantify soluble Aβ aggregates in the brain. We had synthesized a novel fluorinated curcumin derivative with a fixed keto form, named as Shiga-Y51, which exhibited high selectivity to Aβ oligomers in vitro. In this study, we investigated the in vivo detection of Aβ oligomers by fluorine-19 (19F) magnetic resonance imaging (MRI) using Shiga-Y51 in an APP/PS1 double transgenic mouse model of AD. Significantly high levels of 19F signals were detected in the upper forebrain region of APP/PS1 mice compared with wild-type mice. Moreover, the highest levels of Aβ oligomers were detected in the upper forebrain region of APP/PS1 mice in enzyme-linked immunosorbent assay. These findings suggested that 19F-MRI using Shiga-Y51 detected Aβ oligomers in the in vivo brain. Therefore, 19F-MRI using Shiga-Y51 with a 7 T MR scanner could be a powerful tool for imaging Aβ oligomers in the brain.
Keyphrases
- magnetic resonance imaging
- contrast enhanced
- escherichia coli
- wild type
- mouse model
- resting state
- white matter
- diffusion weighted imaging
- computed tomography
- functional connectivity
- high fat diet induced
- cerebral ischemia
- magnetic resonance
- oxidative stress
- positron emission tomography
- skeletal muscle
- insulin resistance
- metabolic syndrome
- high throughput
- mild cognitive impairment
- single cell
- image quality