医学部
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  2. ueda akihiro

ueda akihiro

  (植田 晃広)

Profile Information

Affiliation
Associate Professor, Department of Internal Medicine, Neurology, Fujita Health University Okazaki Medical Center
Degree
博士(医学）(藤田保健衛生大学)
J-GLOBAL ID
201501008162133427
researchmap Member ID
7000012808

Research Areas

 1

Papers

 149
  • Kazuya Kawabata, Fumihiko Banno, Yasuaki Mizutani, Toshiki Maeda, Ryunosuke Nagao, Sayuri Shima, Kazuhiro Murayama, Yoshiharu Ohno, Tetsuya Maeda, Makoto Sasaki, Akihiro Ueda, Mizuki Ito, Hirohisa Watanabe
    Parkinsonism & related disorders, 131 107251-107251, Feb, 2025  
    INTRODUCTION: Progressive supranuclear palsy (PSP) involves midbrain structures, including the red nucleus (RN), an iron-rich region that appears as a high-contrast area on quantitative susceptibility mapping (QSM). RN may serve as a promising biomarker for differentiating parkinsonism. However, RN deformation in PSP remains elusive. This study aimed to evaluate RN deformation in PSP using coronal QSM images and compare them with those of Parkinson's disease (PD) and healthy controls (HC). METHODS: We evaluated the QSM images of 22 patients with PSP, 37 patients with PD, and 43 HC. We developed a grading system to assess RN deformation on coronal QSM images and classified them into three grades. The midbrain and RN volumes were extracted using distinct approaches, and their relationship with grading was investigated. For validation, coronal QSM images of 16 PSP patients from a different institution were assessed. RESULTS: In PSP, 59 % of the patients displayed a flattened RN of grade 3, which we termed a Rice-Grain Appearance. The volume reductions in midbrain and RN were associated with deformation. Differentiation based on the presence of this appearance yielded a specificity of 1.000 (CI: 1.000-1.000) and sensitivity of 0.591 (0.385-0.796) for distinguishing PSP from others. Secondary dataset also showed that 56 % of patients with PSP were classified as grade 3. CONCLUSION: In coronal QSM images, the flattened RN shape appears to be specific to PSP compared to PD and HC and may serve as a marker to help differentiate PSP in future clinical settings.
  • Yoshiki Kawamura, Yasuaki Mizutani, Mao Asakura, Ryunosuke Nagao, Akihiro Ueda, Hirohisa Watanabe, Tetsushi Yoshikawa
    Pediatrics international : official journal of the Japan Pediatric Society, 67(1) e15865, 2025  
  • Ayami Yoshikane, Hiroki Miura, Sayuri Shima, Masaaki Matsunaga, Soichiro Ishimaru, Yuki Higashimoto, Yoshiki Kawamura, Kei Kozawa, Akiko Yoshikawa, Akihiro Ueda, Atsuhiko Ota, Hirohisa Watanabe, Tatsuro Mutoh, Tetsushi Yoshikawa
    Emerging Infectious Diseases, 30(12), Dec, 2024  
  • Xi-Chen Zhu, Yasuaki Mizutani, Reiko Ohdake, Harutsugu Tatebe, Toshiki Maeda, Sayuri Shima, Akihiro Ueda, Mizuki Ito, Shinji Ito, Takahiko Tokuda, Hirohisa Watanabe
    Journal of Parkinson's disease, 14(8) 1533-1542, Nov, 2024  
    BACKGROUND: Recent evidence suggests a link between glycoprotein non-metastatic melanoma protein B (GPNMB) and Parkinson's disease (PD) pathogenesis. Although elevated plasma GPNMB levels associated with disease severity have been reported in PD, cerebrospinal fluid (CSF) alterations remain elusive. OBJECTIVE: To explore CSF GPNMB alterations and its clinical significance in PD. METHODS: This study enrolled 118 sporadic PD patients and 40 controls. We examined the potential associations between CSF GPNMB levels and the clinical characteristics or biomarkers of neurodegenerative pathogenesis. RESULTS: PD patients had higher CSF GPNMB levels than controls (p = 0.0159). In the PD group, CSF GPNMB levels correlated with age (age at examination: rs = 0.2511, p = 0.0061; age at onset: rs = 0.2800, p = 0.0021) and the severity of motor and cognitive dysfunction (MDS-UPDRS III score: rs = 0.1998, p = 0.0347; Mini-Mental State Examination score: rs = -0.1922, p = 0.0370). After correcting for multiple comparisons, the correlation with age at onset remained significant. CSF GPNMB levels were also positively correlated with CSF soluble triggering receptor expressed on myeloid cells 2 (sTREM2) levels in both the PD (rs = 0.3582, p < 0.0001) and control (rs = 0.4743, p = 0.0023) groups. Furthermore, multiple regression analysis revealed CSF sTREM2 level as the strongest determinant of CSF GPNMB levels in the PD group (t-value = 3.49, p = 0.0007). CONCLUSIONS: Elevated CSF GPNMB levels, linked with age and microglial activation, may be a valuable marker for understanding the interplay between aging, neuroinflammation, and PD pathology.
  • Sayuri Shima, Yasuaki Mizutani, Junichiro Yoshimoto, Yasuhiro Maeda, Reiko Ohdake, Ryunosuke Nagao, Toshiki Maeda, Atsuhiro Higashi, Akihiro Ueda, Mizuki Ito, Tatsuro Mutoh, Hirohisa Watanabe
    NPJ Parkinson's disease, 10(1) 170-170, Sep 9, 2024  
    The relationship between reduced serum uric acid (UA) levels and Parkinson's disease (PD), particularly purine metabolic pathways, is not fully understood. Our study compared serum and cerebrospinal fluid (CSF) levels of inosine, hypoxanthine, xanthine, and UA in PD patients and healthy controls. We analyzed 132 samples (serum, 45 PD, and 29 age- and sex-matched healthy controls; CSF, 39 PD, and 19 age- and sex-matched healthy controls) using liquid chromatography-tandem mass spectrometry. Results showed significantly lower serum and CSF UA levels in PD patients than in controls (p < 0.0001; effect size r = 0.5007 in serum, p = 0.0046; r = 0.3720 in CSF). Decreased serum hypoxanthine levels were observed (p = 0.0002; r = 0.4338) in PD patients compared to controls with decreased CSF inosine and hypoxanthine levels (p < 0.0001, r = 0.5396: p = 0.0276, r = 0.2893). A general linear model analysis indicated that the reduced UA levels were mainly due to external factors such as sex and weight in serum and age and weight in CSF unrelated to the purine metabolic pathway. Our findings highlight that decreased UA levels in PD are influenced by factors beyond purine metabolism, including external factors such as sex, weight, and age, emphasizing the need for further research into the underlying mechanisms and potential therapeutic approaches.
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Misc.

 28
  • 朝倉 真生, 水谷 泰彰, 中野 頌子, 林 和孝, 坂野 文彦, 加藤 邦尚, 菊池 洸一, 東 篤宏, 長尾 龍之介, 前田 利樹, 村手 健一郎, 廣田 政古, 石川 等真, 河村 吉紀, 島 さゆり, 植田 晃広, 伊藤 瑞規, 武藤 多津郎, 吉川 哲史, 渡辺 宏久
    臨床神経学, 62(Suppl.) S414-S414, Oct, 2022  
  • Hirohisa Watanabe, Sayuri Shima, Yasuaki Mizutani, Akihiro Ueda, Mizuki Ito
    Brain and nerve = Shinkei kenkyu no shinpo, 74(7) 879-884, Jul, 2022  
    A group of patients with coronavirus disease 2019 (COVID-19) exhibited various persistent or new systemic symptoms, including psychiatric symptoms, sleep disturbances, exercise intolerance, arthralgia, headache, cognitive decline, brain fog, and autonomic symptoms, all of which persisted long after the resolution of infectious symptoms. Several imaging studies have shown that long COVID cases present with decreased glucose metabolism and progressive brain atrophy. Although no single pathological hypothesis thoroughly explains the varied clinical presentations and timings, the following have attracted attention: 1) persistent viral infection, 2) persistent inflammation, 3) involvement of the autoimmune system, and 4) mitochondrial dysfunction. In all these hypotheses, inflammatory cytokines may be involved in orthostatic dysregulation by decreasing the expression and activity of ACE2, consequently changing the blood pressure through vagus nerve hyperactivation. Myopathy and peripheral neuropathy may also be caused by direct infection of the muscles and nerves, hypoxia, mitochondrial damage, and cytokine storm. Furthermore, multiple theories regarding the mechanisms by which systemic inflammatory findings affect the central nervous system have been postulated, including neuroinflammation caused by inflammatory cells crossing the blood-brain barrier via choroid plexus cells and the involvement of various autoantibodies. Despite these findings, no definitive consensus has been reached due to the complexity and diversity of COVID-19 pathophysiology. Thus, it is essential to understand the neurological symptoms and pathophysiology involved in long COVID.
  • 渡辺 宏久, 大嶽 れい子, 水谷 泰彰, 島 さゆり, 伊藤 瑞規, 植田 晃広, 桝田 道人
    画像診断, 42(2) 145-155, Jan 25, 2022  
    ＜文献概要＞TDP-43は主に核内に存在し,RNAの生合成をはじめ様々なプロセスに関与する.TDP-43の核内局在の喪失と異常な翻訳後修飾を受けた不溶化TDP-43の存在を特徴とする一群は,TDP-43proteinopathyと呼ばれ,筋萎縮性側索硬化症と前頭側頭葉変性症が代表的な疾患である.
  • 伊藤 瑞規, 水谷 泰彰, 植田 晃広, 渡辺 宏久
    難病と在宅ケア, 27(10) 51-55, Jan, 2022  
  • 渡辺 宏久, 大嶽 れい子, 水谷 泰彰, 島 さゆり, 伊藤 瑞規, 植田 晃広
    画像診断, 41(14) 1470-1481, Nov 25, 2021  
    ＜文献概要＞認知症の診断は,適切な病歴聴取,神経学的診察,高次脳機能評価,脳画像を評価することで行われる.最近は,血液や髄液のバイオマーカー開発も目覚ましい.脳画像を解釈する上で,認知症の臨床像の特徴,診断基準,臨床病型の多様性,高次脳機能検査結果の解釈方法などを整理することは有益である.
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Presentations

 164
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Research Projects

 4
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