Updated on 2024/11/23

写真a

 
NAKAJIMA Akihiro
 
Organization
University Medical and Dental Hospital Neurology Assistant Professor
Title
Assistant Professor
External link

Degree

  • 博士（医学） ( 2024.3 )

  • 学士(医学) ( 2015.3 )

Research History

  • Niigata University   University Medical and Dental Hospital   Assistant Professor

    2024.4

  • Niigata University   Brain Research Institute   Specially Appointed Assistant Professor

    2020.4 - 2024.3

 

Papers

  • Stage-dependent immunity orchestrates AQP4 antibody-guided NMOSD pathology: a role for netting neutrophils with resident memory T cells in situ. International journal

    Akihiro Nakajima, Fumihiro Yanagimura, Etsuji Saji, Hiroshi Shimizu, Yasuko Toyoshima, Kaori Yanagawa, Musashi Arakawa, Mariko Hokari, Akiko Yokoseki, Takahiro Wakasugi, Kouichirou Okamoto, Hirohide Takebayashi, Chihiro Fujii, Kyoko Itoh, Yo-Ichi Takei, Shinji Ohara, Mitsunori Yamada, Hitoshi Takahashi, Masatoyo Nishizawa, Hironaka Igarashi, Akiyoshi Kakita, Osamu Onodera, Izumi Kawachi

    Acta neuropathologica   147 ( 1 )   76 - 76   2024.4

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    Language：English   Publishing type：Research paper (scientific journal)  

    Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune disease of the CNS characterized by the production of disease-specific autoantibodies against aquaporin-4 (AQP4) water channels. Animal model studies suggest that anti-AQP4 antibodies cause a loss of AQP4-expressing astrocytes, primarily via complement-dependent cytotoxicity. Nonetheless, several aspects of the disease remain unclear, including: how anti-AQP4 antibodies cross the blood-brain barrier from the periphery to the CNS; how NMOSD expands into longitudinally extensive transverse myelitis or optic neuritis; how multiphasic courses occur; and how to prevent attacks without depleting circulating anti-AQP4 antibodies, especially when employing B-cell-depleting therapies. To address these knowledge gaps, we conducted a comprehensive 'stage-dependent' investigation of immune cell elements in situ in human NMOSD lesions, based on neuropathological techniques for autopsied/biopsied CNS materials. The present study provided three major findings. First, activated or netting neutrophils and melanoma cell adhesion molecule-positive (MCAM+) helper T (TH) 17/cytotoxic T (TC) 17 cells are prominent, and the numbers of these correlate with the size of NMOSD lesions in the initial or early-active stages. Second, forkhead box P3-positive (FOXP3+) regulatory T (Treg) cells are recruited to NMOSD lesions during the initial, early-active or late-active stages, suggesting rapid suppression of proinflammatory autoimmune events in the active stages of NMOSD. Third, compartmentalized resident memory immune cells, including CD103+ tissue-resident memory T (TRM) cells with long-lasting inflammatory potential, are detected under "standby" conditions in all stages. Furthermore, CD103+ TRM cells express high levels of granzyme B/perforin-1 in the initial or early-active stages of NMOSD in situ. We infer that stage-dependent compartmentalized immune traits orchestrate the pathology of anti-AQP4 antibody-guided NMOSD in situ. Our work further suggests that targeting activated/netting neutrophils, MCAM+ TH17/TC17 cells, and CD103+ TRM cells, as well as promoting the expansion of FOXP3+ Treg cells, may be effective in treating and preventing relapses of NMOSD.

    DOI： 10.1007/s00401-024-02725-x

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  • Acute respiratory failure caused by brainstem demyelinating lesions in an older patient with an atypical relapsing autoimmune disorder. International journal

    Shoko Hongo, Hiroshi Shimizu, Etsuji Saji, Akihiro Nakajima, Kouichirou Okamoto, Izumi Kawachi, Osamu Onodera, Akiyoshi Kakita

    Neuropathology : official journal of the Japanese Society of Neuropathology   2024.4

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    Language：English  

    An 84-year-old man presented with somnolence, dysphagia, and right hemiplegia, all occurring within a month, approximately one year after initial admission due to subacute, transient cognitive decline suggestive of acute disseminated encephalomyelitis involving the cerebral white matter. Serial magnetic resonance imaging (MRI) studies over that period revealed three high-intensity signal lesions on fluid-attenuated inversion recovery images, appearing in chronological order in the left upper and left lower medulla oblongata and left pontine base. Despite some clinical improvement following methylprednisolone pulse therapy, the patient died of respiratory failure. Autopsy revealed four fresh, well-defined lesions in the brainstem, three of which corresponded to the lesions detected radiologically. The remaining lesion was located in the dorsal medulla oblongata and involved the right solitary nucleus. This might have appeared at a later disease stage, eventually causing respiratory failure. Histologically, all four lesions showed loss of myelin, preservation of axons, and infiltration of lymphocytes, predominantly CD8-positive T cells, consistent with the histological features of autoimmune demyelinating diseases, particularly the confluent demyelination observed in the early and acute phases of multiple sclerosis (MS). In the cerebral white matter, autoimmune demyelination appeared superimposed on ischemic changes, consistent with the cerebrospinal fluid (CSF) and MRI findings on initial admission. No anti-AQP4 or MOG antibodies or those potentially causing autoimmune encephalitis/demyelination were detected in either the serum or CSF. Despite several similarities to MS, such as the relapsing-remitting disease course and lesion histology, the entire clinicopathological picture in the present patient, especially the advanced age at onset and development of brainstem lesions in close proximity within a short time frame, did not fit those of MS or other autoimmune diseases that are currently established. The present results suggest that exceptionally older individuals can be affected by an as yet unknown inflammatory demyelinating disease of the CNS.

    DOI： 10.1111/neup.12976

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  • [A case of neuralgic amyotrophy with extension disturbance of fingers after Cushing's syndrome remission].

    Akihiro Nakajima, Takao Fukushima, Hideki Mori, Hiroaki Nozaki, Kunihiko Makino

    Rinsho shinkeigaku = Clinical neurology   62 ( 8 )   632 - 636   2022.8

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    Language：Japanese   Publishing type：Research paper (scientific journal)  

    We describe a 57-year-old female patient who experienced hypercortisolemia caused by adrenal Cushing's syndrome. Two months post-adrenalectomy, she developed acute severe bilateral pain starting in her fingers and spreading up her arms. In the subsequent two weeks, the patient presented upper extremity patchy paralysis with extension disturbance of fingers. In the following two months, she experienced atrophy of the muscles in the hands and joint contracture. Consequently, we diagnosed her with neuralgic amyotrophy. Nerve conduction studies showed low compound muscle action potential of all the peripheral nerves in the forearms, suggesting motor neuron axonopathy. Gadolinium-enhanced MRI and ultrasound studies did not reveal any abnormalities in the brachial plexus and peripheral nerves of the forearms. The patient tested positive for anti-GalNAc-GD1a-IgM antibodies and received intravenous immunoglobulin 6 months after the onset of symptoms, which resulted in reduction of pain, muscle weakness, and contractures. This rare case of potentially immune-mediated bilateral patchy paralysis may have important implications in the understanding of clinical and pathological heterogenicity of neuralgic amyotrophy.

    DOI： 10.5692/clinicalneurol.cn-001759

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  • 出血性病変が検出されずに広範な脳病変に至ったアミロイドβ関連血管炎の1例

    畠野 雄也, 須貝 章弘, 山岸 拓磨, 中島 章博, 柿田 明美, 小野寺 理

    臨床神経学   60 ( 3 )   187 - 192   2020.3

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    Language：Japanese   Publisher：(一社)日本神経学会  

    アミロイドβ関連血管炎(amyloid β-related angiitis)では、皮質や皮質下の微小出血や脳表ヘモジデリンの沈着が、脳MRI上の重要な所見である。我々は、治療前にはこれらの所見を呈さなかったアミロイドβ関連血管炎を提示する。症例は75歳女性。右同名半盲と失語で発症し、昏睡に至った。脳MRIでは、びまん性の軟髄膜造影病変と散在性のDWI高信号病変を認めたが、T2*WIでは微小出血は検出されなかった。病理所見からアミロイドβ関連血管炎と診断した。ステロイド治療により画像所見、臨床症状ともに改善した。治療後のsusceptibility-weighted imaging(SWI)では多数の微小出血を認めた。アミロイドβ関連血管炎の非侵襲的診断のために、微小出血以外の画像の特徴を集積すべきである。(著者抄録)

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    Other Link： https://search.jamas.or.jp/default/link?pub_year=2020&ichushi_jid=J01550&link_issn=&doc_id=20200310190003&doc_link_id=1390565134843079680&url=https%3A%2F%2Fcir.nii.ac.jp%2Fcrid%2F1390565134843079680&type=CiNii&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00003_3.gif

  • Tubulointerstitial nephritis and Fanconi syndrome in a patient with primary Sjögren's syndrome accompanied by antimitochondrial antibodies: A case report and review of the literature. International journal

    Takako Saeki, Akihiro Nakajima, Tomoyuki Ito, Takuma Takata, Naofumi Imai, Kazuhiro Yoshita, Hideyuki Kabasawa, Hajime Yamazaki, Ichiei Narita

    Modern rheumatology   28 ( 5 )   897 - 900   2018.9

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    Language：English   Publishing type：Research paper (scientific journal)  

    We describe a 53-year-old woman with primary Sjögren's syndrome and tubulointerstitial nephritis showing distal renal tubular acidosis and Fanconi syndrome. The patient showed high serum IgM levels and positivity for antimitochondrial antibodies, although her liver function was in normal range. According to our literature review, 75% of patients with tubulointerstitial nephritis who were positive for antimitochondrial antibodies showed Fanconi syndrome, suggesting that these antibodies may directly be associated with the pathophysiology of Fanconi syndrome.

    DOI： 10.3109/14397595.2016.1174422

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