7 results on '"Aya Midori Tokumaru"'
Search Results
2. High sensitivity of asymmetric 18F-THK5351 PET abnormality in patients with corticobasal syndrome
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Masanori Kurihara, Kenji Ishibashi, Tomoyasu Matsubara, Keiko Hatano, Ryoko Ihara, Mana Higashihara, Masashi Kameyama, Aya Midori Tokumaru, Katsuhiko Takeda, Yasushi Nishina, Kazutomi Kanemaru, Kenji Ishii, and Atsushi Iwata
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Medicine ,Science - Abstract
Abstract Corticobasal syndrome (CBS) is characterized by symptoms related to the asymmetric involvement of the cerebral cortex and basal ganglia. However, early detection of asymmetric imaging abnormalities can be challenging. Previous studies reported asymmetric 18F-THK5351 PET abnormalities in CBS patients, but the sensitivity for detecting such abnormalities in larger patient samples, including early-stage cases, remains unclear. Patients clinically diagnosed with CBS were recruited. All patients displayed asymmetric symptoms in the cerebral cortex and basal ganglia. Asymmetric THK5351 PET abnormalities were determined through visual assessment. Brain MRI, perfusion SPECT, and dopamine transporter (DAT) SPECT results were retrospectively reviewed. The 15 patients had a median age of 72 years (59–86 years) and a disease duration of 2 years (0.5–7 years). Four patients met the probable and 11 met the possible CBS criteria according to Armstrong criteria at the time of PET examination. All patients, including early-stage cases, exhibited asymmetric tracer uptake contralateral to their symptom-dominant side in the cerebral cortex/subcortical white matter and striatum (100%). The sensitivity for detecting asymmetric imaging abnormalities contralateral to the symptom-dominant side was 86.7% for brain MRI, 81.8% for perfusion SPECT, and 90% for DAT SPECT. White matter volume reduction was observed in the subcortical region of the precentral gyrus with increased THK5351 uptake, occurring significantly more frequently than gray matter volume reduction. THK5351 PET may be a sensitive imaging technique for detecting asymmetric CBS pathologies, including those in early stages.
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- 2023
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3. Frequency of anti-IgLON5 disease in patients who meet the clinical diagnostic criteria for progressive supranuclear palsy/corticobasal syndrome (S22.010)
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Yoya Ono, Akira Takekoshi, Nobuaki Yoshikura, Hiroshi Takigawa, Ikuko Aiba, Ritsuko Hanajima, Hisanori Kowa, Masato Kanazawa, Takahiko Tokuda, Aya Midori Tokumaru, Mitsuya Morita, Kazuko Hasegawa, Kenji Nakashima, Takeshi Ikeuchi, Akio Kimura, and Takayoshi Shimohata
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- 2023
4. CSF P-Tau181 and Other Biomarkers in Patients With Neuronal Intranuclear Inclusion Disease
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Masanori Kurihara, Hiroki Komatsu, Renpei Sengoku, Mari Shibukawa, Satoru Morimoto, Tomoyasu Matsubara, Akira Arakawa, Makoto Orita, Kenji Ishibashi, Akihiko Mitsutake, Shota Shibata, Hiroyuki Ishiura, Kaori Adachi, Kensuke Ohse, Keiko Hatano, Ryoko Ihara, Mana Higashihara, Yasushi Nishina, Aya Midori Tokumaru, Kenji Ishii, Yuko Saito, Shigeo Murayama, Kazutomi Kanemaru, and Atsushi Iwata
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Neurology (clinical) - Abstract
CSF tau phosphorylated at threonine 181 (p-tau181) is a widely used biomarker for Alzheimer's disease (AD) and has recently been regarded to reflect amyloid-beta and/or p-tau deposition in the AD brain. Neuronal intranuclear inclusion disease (NIID) is a neurodegenerative disease characterized by intranuclear inclusions in neurons, glial cells, and other somatic cells. Symptoms include dementia, neuropathy, and others. CSF biomarkers were not reported. The objective of this study was to investigate whether CSF biomarkers including p-tau181 are altered in patients with NIID.This was a retrospective observational study. CSF concentrations of p-tau181, total tau, amyloid-beta 1-42 (Aβ42), monoamine metabolites homovanillic acid (HVA), and 5-hydroxyindole acetic acid (5-HIAA) were compared between 12 patients with NIID, 120 patients with Alzheimer's clinical syndrome biologically confirmed based on CSF biomarker profiles, and patients clinically diagnosed with other neurocognitive disorders (dementia with Lewy bodies [DLB], 24; frontotemporal dementia [FTD], 13; progressive supranuclear palsy [PSP], 21; and corticobasal syndrome [CBS], 13). Amyloid PET using Pittsburgh compound B (PiB) was performed in six NIID patients.The mean age of patients with NIID, AD, DLB, FTD, PSP, and CBS were 71.3, 74.6, 76.8, 70.2, 75.5, and 71.9 years old, respectively. CSF p-tau181 was significantly higher in NIID (72.7 ± 24.8 pg/mL) compared to DLB, PSP, and CBS and was comparable between NIID and AD. CSF p-tau181 was above the cutoff value (50.0 pg/mL) in 11 of 12 NIID patients (91.7%). Within these patients, only two patients showed decreased CSF Aβ42, and these patients showed negative or mild local accumulation in PiB PET, respectively. PiB PET scans were negative in the remaining 4 patients tested. The proportion of patients with increased CSF p-tau181 and normal Aβ42 (A-T+) was significantly higher in NIID (75%) compared to DLB, PSP, and CBS (4.2%, 4.8%, and 7.7%, respectively). CSF HVA and 5-HIAA concentrations were significantly higher in patients with NIID compared to disease controls.CSF p-tau181 was increased in patients with NIID without amyloid accumulation. Although the deposition of p-tau has not been reported in NIID brains, molecular mechanism of tau phosphorylation or secretion of p-tau may be altered in NIID.
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- 2022
5. CSF p-tau181 Increases in Patients with Neuronal Intranuclear Inclusion Disease without Amyloid Burden
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Masanori Kurihara, Hiroki Komatsu, Renpei Sengoku, Mari Shibukawa, Satoru Morimoto, Tomoyasu Matsubara, Akira Arakawa, Makoto Orita, Kenji Ishibashi, Akihiko Mitsutake, Shota Shibata, Hiroyuki Ishiura, Kaori Adachi, Kensuke Ohse, Keiko Hatano, Ryoko Ihara, Mana Higashihara, Yasushi Nishina, Aya Midori Tokumaru, Kenji Ishii, Yuko Saito, Shigeo Murayama, Kazutomi Kanemaru, and Atsushi Iwata
- Abstract
Background and ObjectivesCSF tau phosphorylated at threonine 181 (p-tau181) is a widely used biomarker for Alzheimer’s disease (AD) and has recently been regarded to reflect amyloid-beta (Aβ) and/or p-tau deposition in the AD brain. Although it is important to know how this biomarker reacts in other neurocognitive diseases, CSF p-tau181 in patients with neuronal intranuclear inclusion disease (NIID) has not been studied.MethodsCSF concentrations of p-tau181, total tau, amyloid-beta 1-42 (Aβ42), monoamine metabolites homovanillic acid (HVA), and 5-hydroxyindole acetic acid (5-HIAA) were compared between 12 patients with NIID, 120 patients with symptomatic AD biologically confirmed based on CSF biomarker profiles, and patients clinically diagnosed with other neurocognitive disorders (dementia with Lewy bodies [DLB], 24; frontotemporal dementia [FTD], 13; progressive supranuclear palsy [PSP], 21; and corticobasal syndrome [CBS], 13). Amyloid PET using Pittsburgh compound B (PiB) was performed in six NIID patients.ResultsCSF p-tau181 concentration was significantly higher in NIID (72.7 ± 24.8 pg/mL) compared to DLB, PSP, and CBS and was comparable between NIID and AD. CSF p-tau181 was above the cutoff value (50.0 pg/mL) in 11 of 12 NIID patients (91.7%). Within these patients, only two patients showed decreased CSF Aβ42, and these patients showed negative or mild local accumulation in PiB PET, respectively. PiB PET scans were negative in the remaining 4 patients tested. CSF HVA and 5-HIAA concentrations were significantly higher in patients with NIID compared to disease controls.DiscussionCSF p-tau181 was increased in patients with NIID without amyloid accumulation. Although the deposition of p-tau has not been reported in NIID brains, molecular mechanism of tau phosphorylation or secretion of p-tau may be altered in NIID.
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- 2022
6. Diffusion-Weighted Imaging is Key to Diagnosing Specific Diseases
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Yuko Saito, Shigeo Murayma, and Aya Midori Tokumaru
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Adult ,Pathology ,medicine.medical_specialty ,Neuroimaging ,Disease ,Creutzfeldt-Jakob Syndrome ,030218 nuclear medicine & medical imaging ,Leukoencephalopathy ,03 medical and health sciences ,NEURONAL INTRANUCLEAR INCLUSION DISEASE ,0302 clinical medicine ,Leukoencephalopathies ,medicine ,Humans ,Radiology, Nuclear Medicine and imaging ,Medical diagnosis ,Axonal spheroids ,business.industry ,medicine.disease ,Magnetic Resonance Imaging ,Diffusion Magnetic Resonance Imaging ,nervous system ,Diffuse leukoencephalopathy ,business ,030217 neurology & neurosurgery ,Diffusion MRI - Abstract
This article reviews diseases for which persistent signal abnormalities on diffusion-weighted imaging are the key to their diagnosis. Specifically, updated knowledge regarding the neuroimaging patterns of the following diseases is summarized: sporadic Creutzfeldt-Jakob disease, neuronal intranuclear inclusion disease, and hereditary diffuse leukoencephalopathy with axonal spheroids-colony-stimulating factor receptors/adult-onset leukoencephalopathy with axonal spheroids and pigmented glia. In addition, their differential diagnoses; clinical manifestations; and pathologic, genetic, and imaging correlates are discussed.
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- 2021
7. Neuroimaging Diagnosis for Alzheimer's Disease and Other Dementias
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Hiroshi Matsuda, Takashi Asada, Aya Midori Tokumaru, Hiroshi Matsuda, Takashi Asada, and Aya Midori Tokumaru
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- Diagnostic imaging, Older people, Brain--Imaging, Alzheimer's disease--Diagnosis--Imaging, Dementia--Diagnosis--Imaging, Nervous system--Imaging
- Abstract
This book describes the latest modalities such as tau PET imaging for diagnosis of Alzheimer's disease and other dementias, and also provides information on handling and analyzing imaging data that is not found in other books. In addition, it introduces routine imaging studies in the management of dementia in Japan. The prevalence of dementia has increased over the past few decades, either because of greater awareness and more accurate diagnosis, or because increased longevity has created a larger population of the elderly, the age group most commonly affected. Although only clinical assessment can lead to a diagnosis of dementia, neuroimaging in dementia is recommended by most clinical guidelines, and its adjunct role has traditionally been to exclude a mass lesion rather than to support a specific diagnosis. Neuroimaging may be also helpful for developing new strategies to achieve diagnoses as early as possible for therapies aimed at slowing the progression of neurodegenerative diseases manifesting dementia. Under these conditions, all clinicians and researchers who are involved in neuroimaging for dementia should decide which patients to scan, when imaging patients is most useful, which modality to use, how to handle imaging data from many institutions, and which analytical tool to use. This edition comprises contributions from leading Japanese experts in their fields.
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- 2017
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