Tohoku University · Medicine
Professor Ryuichi Harada's research lab specializes in the development and application of novel positron emission tomography (PET) radiotracers for the in vivo imaging of neurodegenerative diseases. The lab focuses on targeting key neuropathological features such as tau pathology, astrogliosis, and amyloid burden, with particular emphasis on creating selective and specific tracers like 18F-THK5351 and 18F-SMBT-1. Their work bridges molecular imaging, neuroscience, and clinical diagnostics to improve early detection, differential diagnosis, and therapeutic monitoring in Alzheimer’s disease and other tauopathies. The lab also investigates the role of glial activation in neuroinflammation, aiming to integrate glial imaging with amyloid and tau PET for a comprehensive understanding of disease progression.
Figures are computed from collected data and may differ slightly.
(18)F-THK5351 is a useful PET tracer for the early detection of neurofibrillary pathology in AD patients.
Clinical PET studies using <sup>18</sup>F-THK5351 have demonstrated significant tracer retention in sites susceptible to tau burden in Alzheimer disease (AD). However, the in vivo PET signal to reflect tau aggregates remains controversial. <b>Methods:</b> We examined the spatial pattern of tracer binding, amyloid-β, tau, and gliosis in an autopsy-confirmed AD patient who underwent <sup>18</sup>F-THK5351 and <sup>11</sup>C-Pittsburgh compound B PET before death. <b>Results:</b> Regional in vivo <
Tau deposition is one of the neuropathological hallmarks in Alzheimer's disease as well as in other neurodegenerative disorders called tauopathies. Recent efforts to develop selective tau radiopharmaceuticals have allowed the visualization of tau deposits in vivo. In vivo tau imaging allows the assessment of the regional distribution of tau deposits in a single human subject over time for determining the pathophysiology of tau accumulation in aging and neurodegenerative conditions as well as for
Reactive astrocytes play a key role in the pathogenesis of various neurodegenerative diseases. Monoamine oxidase-B (MAO-B) is one of the promising targets for the imaging of astrogliosis in the human brain. A novel selective and reversible MAO-B tracer, (<i>S</i>)-(2-methylpyrid-5-yl)-6-[(3-<sup>18</sup>F-fluoro-2-hydroxy)propoxy]quinoline (<sup>18</sup>F-SMBT-1), was successfully developed via lead optimization from the first-generation tau PET tracer <sup>18</sup>F-THK-5351. <b>Methods:</b> SM
Many neurodegenerative diseases are neuropathologically characterized by neuronal loss, gliosis, and the deposition of misfolded proteins such as β-amyloid (Aβ) plaques and tau tangles in Alzheimer's disease (AD). In postmortem AD brains, reactive astrocytes and activated microglia are observed surrounding Aβ plaques and tau tangles. These activated glial cells secrete pro-inflammatory cytokines and reactive oxygen species, which may contribute to neurodegeneration. Therefore, <i>in vivo</i> ima
Neurodegenerative diseases characterized by pathological protein accumulation in cells are termed "proteinopathies." Although various protein aggregates share cross-β-sheet structures, actual conformations vary among each type of protein deposit. Recent progress in the development of radiotracers for positron emission tomography (PET) has enabled the visualization of protein aggregates in living brains. Amyloid PET tracers have been developed, and are widely used for the diagnosis of Alzheimer's
Tau PET tracers are expected to be sufficiently sensitive to track the progression of age-related tau pathology in the medial temporal cortex. The tau PET tracer <i>N</i>-(4-[<sup>18</sup>F]fluoro-5-methylpyridin-2-yl)-7-aminoimidazo[1,2-a]pyridine ([<sup>18</sup>F]SNFT-1) has been successfully developed by optimizing imidazo[1,2-a]pyridine derivatives. We characterized the binding properties of [<sup>18</sup>F]SNFT-1 using a head-to-head comparison with other reported <sup>18</sup>F-labeled tau
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