KEIO RESEARCHERS INFORMATION SYSTEM

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• Toshihide Kurihara is an Associate Professor of Ophthalmology at Keio University, Tokyo, Japan. He has also been appointed as an Adjunct Assistant Professor at the Scripps Research Institute (TSRI) in La Jolla, CA, USA. He received his M.D. degree from the Faculty of Medicine, University of Tsukuba, Ibaraki, Japan, in 2001. He completed his ophthalmology residency at Keio University Hospital in 2005, and obtained his Ph.D. degree under the supervision of Professor Kazuo Tsubota from Keio University Graduate School of Medicine in 2009. Dr. Kurihara did his postdoctoral training under the mentorship of Professor Martin Friedlander at TSRI. His research interest is hypoxia responses in development, physiology, and pathophysiology of the retina. Editorial Board　Member: BioMed Research International, Journal of Ophthalmology, and Case Reports in Ophthalmological Medicine

Career 【 Display / hide 】

Career 【 Display / hide 】

• 2001.04

  -

  2003.03

  Keio University Hospital, Department of Ophthalmology, Resident

• 2002.07

  -

  2003.06

  National Kasumigaura Hospital, Department of Ophthalmology, Resident

• 2003.04

  -

  2004.03

  Keio University Hospital, Department of Ophthalmology, Clinical Fellow

• 2004.01

  -

  2005.03

  Tokyo Saiseikai Central Hospital, Ophthalmology, Clinical Fellow

• 2005.04

  -

  2009.03

  Keio University Graduate School of Medicine, Doctoral Course

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Academic Background 【 Display / hide 】

Academic Background 【 Display / hide 】

• 1995.04

  -

  2001.03

  University of Tsukuba, School of Medicine

  University, Graduated

• 2005.04

  -

  2009.03

  Keio University, Graduate School of Medicine

  Graduate School, Completed

Academic Degrees 【 Display / hide 】

Academic Degrees 【 Display / hide 】

• PhD in Medicine, Keio University, Coursework, 2009.03

  Angiotensin 2 type 1 receptor signaling contributes to synaptophysin degradation and neuronal dysfunction in the diabetic retina

Research Areas 【 Display / hide 】

Research Areas 【 Display / hide 】

• Life Science / Ophthalmology (Ophthalmology)

Papers 【 Display / hide 】

Papers 【 Display / hide 】

• Layer-specific retinal remodeling after epiretinal membrane surgery assessed with ultra-widefield optical coherence tomography

  Yuda T, Tomita Y†, Araki R, Zhang Y, Jiang X, Hayashi I, Kunimi H, Ban N, Shinoda H, Kurihara T, Negishi K

  AJO International. (Elsevier BV)  3 ( 4 ) 100317 2026.12

  Accepted,  ISSN  2950-2535

  　View Summary

  Objective/purpose: To investigate the spatial heterogeneity of early postoperative retinal remodeling following pars plana vitrectomy (PPV) for epiretinal membrane (ERM) using layer-by-layer ultra-widefield optical coherence tomography (UWF-OCT) to evaluate both the central and peripheral retina. Design: Retrospective observational study. Subjective, participants, and/or controls: Thirty eyes of 30 patients who underwent PPV for ERM. Methods, intervention, or testing: We acquired swept-source UWF-OCT images preoperatively and at 1 month postoperatively. Using automated segmentation, the analysis area was divided into a central 5-mm diameter region and 8 peripheral sectors extending to an 18-mm diameter. We quantified regional changes in total retinal thickness, the thickness of 5 segmented retinal layers, retinal vessel density, and choroidal thickness across the central and peripheral subfields. Results: The mean age was 68.0 ± 8.0 years, and 29 of 30 eyes (96.7%) underwent combined phacovitrectomy. Visual acuity improved from 0.19 ± 0.19 to 0.05 ± 0.12 logarithm of the minimum angle of resolution at 1 month (P < 0.001). Central total retinal thickness decreased significantly (P < 0.001), primarily because of thinning of the retinal nerve fiber layer, ganglion cell layer–inner plexiform layer, and inner nuclear layer–outer plexiform layer. In contrast, total retinal thickness increased significantly in 4 of the 8 peripheral sectors (L2, L6, L7, and L8; P < 0.0056), and the inner segment/outer segment junction–retinal pigment epithelium compartment thickened significantly across all 8 peripheral sectors. The overall time-by-region interaction for retinal vessel density was not significant (P = 0.105), although an isolated increase in L4 met the Bonferroni-adjusted threshold (P = 0.005). No significant postoperative changes were detected in choroidal thickness in any region. Conclusions: Early after epiretinal membrane surgery, retinal remodeling appears spatially heterogeneous, with central inner retinal thinning and peripheral thickening of the inner segment/outer segment junction–retinal pigment epithelium compartment. Layer-specific ultra-widefield optical coherence tomography may complement macular metrics in postoperative structural assessment. The biological basis and functional relevance of these peripheral changes require confirmation in larger longitudinal studies.

  • Access to Document (DOI)

• Photobiology in ophthalmology: from evolutionary adaptation to translational therapeutics

  Kurihara T†

  Jpn J Ophthal. (Springer Science and Business Media LLC)   2026.09

  Lead author, Last author, Corresponding author, Accepted,  ISSN  0021-5155

  　View Summary

  Abstract
  
  Life has evolved under continuous exposure to solar light, and the emergence of the eye during the Cambrian period is thought to have accelerated biological diversification. Beyond vision, light acts as a biological regulator of metabolism and tissue organization. To elucidate ocular disease mechanisms and develop new therapies, we have investigated how light is sensed by the eye and coupled to physiological and pathological responses. This review reexamines the eye as a photoreceptive organ and summarizes recent advances showing how light input governs retinal metabolism, refractive development, and visual restoration. First, we describe how retinal light reception is linked to oxygen-dependent metabolic control. As one of the most oxygen-demanding tissues, the retina relies on hypoxia-inducible factor (HIF) signaling to coordinate angiogenesis, mitochondrial metabolism, fibrosis, and neuronal survival. Beyond pathological neovascularization, disrupted light-metabolic coupling contributes to neurodegeneration and subretinal scarring. Screening of natural compounds identified HIF regulators with therapeutic efficacy, and optical approaches were developed to detect hypoxia-induced intraocular cytokines noninvasively. Second, we show that environmental light regulates ocular growth in ways beyond image formation. Violet light activates nonvisual photoreception via OPN5-expressing retinal ganglion cells, engaging an OPN5-EGR1 pathway that preserves choroidal thickness and suppresses axial elongation through coordinated retina-brain-choroid-sclera interactions. Third, we demonstrate that light itself becomes therapeutic through optogenetic visual restoration. Chimeric rhodopsins confer high-sensitivity light responsiveness to surviving inner retinal neurons and have recently entered first-in-human clinical evaluation for advanced retinitis pigmentosa. These findings establish photobiology as a unifying framework for translational ophthalmology.

  • Access to Document (DOI)

• Chimeric Gtacr2 Restores ON Responses Involving Hyperpolarization-Activated Channels In A Mouse Model Of Retinal Degeneration

  Li M*, Suga A*, Hososhima S, Tsunoda SP, Yoshida K, Negishi K, Kandori H, Katada Y, Kurihara T†

  SSRN (Elsevier BV)   2026.09

  Last author, Corresponding author

  　View Summary

  Background: Optogenetic tools have been extensively investigated in basic and clinical research to restore vision in advanced retinal degeneration. Although microbial ion channel opsins, mammalian G protein-coupled receptor opsins, and chimeric opsins combining domains from different molecules have been reported, how these domain combinations affect opsin function and retinal responses remains poorly understood.&lt;br&gt;&lt;br&gt;Methods:We engineered a chimeric GtACR2 (chGtACR2) containing bovine rhodopsin cytoplasmic loops and delivered it to the retinas of rd1 mice. light-induced responses of GtACR2 and chGtACR2 in the cell line and retinas were compared by patch-clump and multielectrode array, respectively. Visual acuity and contrast sensitivity of chGtACR2-treated mice were examined by optomotor response test. Endogenous ion channels involved in the chGtACR2-induced light responses were tested by pharmacological blockade.&lt;br&gt;&lt;br&gt;Findings: Although patch-clamp recordings confirmed that chGtACR2 functioned as a light-gated chloride channel that induced membrane hyperpolarization, multielectrode array recordings revealed chGtACR2-induced ON-like responses in retinal ganglion cells across the tested stimulus intensities, with increases in the number of responsive units and their firing rates. Visual acuity and contrast sensitivity were improved in vivo. Hyperpolarization-activated cyclic nucleotide-gated (HCN) channel activity contributed to these ON-like responses.&lt;br&gt;&lt;br&gt;Interpretation:These findings suggest that endogenous HCN channel activity can influence retinal responses to an introduced optogenetic tool and highlight the potential of modifying cytoplasmic domains to alter the functional properties of microbial opsins.&lt;br&gt;&lt;br&gt;Funding: AMED-CRST (JP22gm1510007), JSPS KAKENHI (JP25K12842, JP26H00468, and JP24K12796), and SPRING(JPMJSP2123).

  • Access to Document (DOI)

• Nicotinamide Mononucleotide Attenuates Inflammatory Activation, Choroidal Neovascularization, and Lesion-Associated Remodeling

  Wang J, Osada H, Chen S, Yamaguchi S, Hayashi K, Negishi K, Kurihara T, Ban N†

  Invest Ophthalmol Vis Sci. (Association for Research in Vision and Ophthalmology (ARVO))  67 ( 10 ) 59 2026.08

  Accepted,  ISSN  1552-5783

  　View Summary

  PURPOSE. To evaluate the therapeutic potential of nicotinamide mononucleotide (NMN) for modulating the neurovascular inflammatory microenvironment and blunting tissue remodeling in neovascular age-related macular degeneration (nAMD). METHODS. A laser-induced choroidal neovascularization (CNV) model was established in C57BL/6J mice, and CNV lesion size was quantified on RPE/choroid flat mounts. Immunostaining evaluated myeloid cell accumulation and fibrosis-associated remodeling. Quantitative RT-PCR and Western blotting assessed inflammatory/angiogenic gene expression and signaling activation in the retina and RPE/choroid. In vitro, lipopolysaccharide (LPS)–stimulated bEnd.3 and primary mouse RPE cells and TGF-β–stimulated THP-1–derived macrophage cells were used to model inflammatory and profibrotic responses. RESULTS. NMN treatment significantly reduced CNV size in the laser-induced CNV model. This was accompanied by decreased myeloid cell accumulation within CNV lesions. NMN attenuated inflammatory and angiogenesis-related gene expression in the RPE/choroid and neural retina and reduced downstream signaling activation. In vitro, NMN suppressed LPS-induced inflammatory and proangiogenic responses in primary RPE cells and bEnd.3 endothelial cells and inhibited NF-κB activation. NMN further attenuated tissue remodeling, as shown by reduced collagen I–positive area under prolonged and delayed dosing regimens, together with decreased F4/80-positive area and α–smooth muscle actin–positive area within CNV lesions. In TGF-β–induced THP-1–derived macrophage cells, NMN suppressed profibrotic responses. CONCLUSIONS. Our findings indicate that NMN reduces inflammatory signaling and alleviates the inflammatory microenvironment in CNV, accompanied by decreased angiogenesis-related gene expression and fibrosis-related remodeling. By attenuating inflammatory activation and tissue remodeling processes, NMN warrants further evaluation as an adjunctive approach to limit CNV progression and late-stage tissue remodeling in nAMD.

  • Access to Document (DOI)

• Long-term visual outcomes and development of retinal pigment epithelial and outer retinal atrophy in neovascular age-related macular degeneration: a comparison of conventional and novel classifications

  Hazra D, Tomita Y†, Uchida A, Kato S, Nagai N, Suzuki M, Minami S, Kunimi H, Ban N, Kurihara T, Shinoda H, Ozawa Y, Negishi K

  BMC Ophthalmol. (Springer Science and Business Media LLC)  26 ( 1 ) 531 2026.08

  Accepted

  　View Summary

  Abstract
  
  Background
  
  Retinal pigment epithelial and outer retinal atrophy (RORA) and complete RORA (cRORA) are major determinants of long-term vision in neovascular age-related macular degeneration (nAMD), but their development across subtypes is poorly defined, especially in Asian populations, in whom pachychoroid-driven disease is common. We compared long-term visual outcomes and atrophy burden between the conventional and novel nAMD classifications.
  
  Methods
  
  One hundred twenty eyes of 120 treatment-naïve patients with nAMD followed at least six years were classified by conventional (typical nAMD [tAMD], polypoidal choroidal vasculopathy [PCV], retinal angiomatous proliferation [RAP]) and novel (drusen type, pachychoroid type, mixed type, other type) schemes. All eyes received three loading anti-VEGF injections followed by a pro re nata regimen. RORA within the central 1 mm was graded on optical coherence tomography; lesions ≥ 250 μm were defined as cRORA. Visual acuity (VA) retention, atrophy prevalence, and VA around atrophy onset were assessed.
  
  Results
  
  Mean age was 78.0 ± 9.2 years and overall VA retention was 71%. VA retention did not differ among conventional subtypes, but under the novel classification was significantly lower in the drusen type and higher in the pachychoroid type ( P  &lt; 0.01). VA declined significantly after both RORA and cRORA onset (both P  &lt; 0.001). Final RORA/cRORA prevalence was 44.4%/29.6% in tAMD, 50.0%/28.3% in PCV, 83.3%/50.0% in RAP and 76.9%/61.5% in the drusen type, in which cRORA was highest ( P  &lt; 0.05).
  
  Conclusions
  
  The novel classification distinguished long-term visual outcomes that the conventional classification did not: the drusen type showed the poorest VA retention and highest cRORA prevalence, whereas the pachychoroid type fared best.

  • Access to Document (DOI)

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Papers, etc., Registered in KOARA 【 Display / hide 】

Papers, etc., Registered in KOARA 【 Display / hide 】

• Investigating mechanisms of axial elongation control by non-visual opsin

  Kurihara, Toshihide

  科学研究費補助金研究成果報告書 2023

• Establishment of a novel visual restoration technology utilizing optogenetics

  Kurihara, Toshihide

  福澤諭吉記念慶應義塾学事振興基金事業報告集 (福澤基金運営委員会)  2023

• Establishment of novel therapeutic technology utilizing optogenetics

  Kurihara, Toshihide

  福澤諭吉記念慶應義塾学事振興基金事業報告集 (福澤基金運営委員会)  2021

• Development of retinal disease regulation from prevention to therapeutic technology targeting hypoxia responses

  Kurihara, Toshihide

  科学研究費補助金研究成果報告書 2020

• A novel prevention and treatment method of ocular aging by targeting sirtuins

  Kurihara, Toshihide

  科学研究費補助金研究成果報告書 2019

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Reviews, Commentaries, etc. 【 Display / hide 】

Reviews, Commentaries, etc. 【 Display / hide 】

• 眼疾患と臓器連関 －腸・腎・脳ネットワークから再定義される眼の全身医学的意義－

  栗原俊英

  Medical Science Digest 52 ( 6 ) 340 - 343 2026.05

  Lead author, Last author, Corresponding author

• Erratum: Correction: Clinical implications of systolic blood pressure for diabetic retinopathy across HbA1c levels in a Japanese population (Scientific reports (2026) 16 1 PII: 11395 DOI: 10.1038/s41598-026-35660-w.)

  Sasaki M., Ofuji Y., Hanyuda A., Kurihara T., Tomita Y., Mori K., Ozawa N., Ozawa Y., Yamagishi K., Yuki K., Sawada N., Tsubota K., Negishi K., Tsugane S., Iso H.

  Scientific Reports 16 ( 1 )  2026.04

  • Access to Document (DOI)

• Erratum: Choroidal Mast Cells and Their Degranulation Are a Pivotal Trigger for Myopia Development (Invest Ophthalmol Vis Sci. (2025) 66:14 (22) DOI: 10.1167/iovs.66.14.22)

  Shi J., Ikeda S.I., Fukuchi T., Chen J., Gettinger K., Imanishi S., Negishi K., Tsubota K., Kurihara T.

  Investigative Ophthalmology and Visual Science 66 ( 15 )  2025.12

  ISSN  01460404

  　View Summary

  The article was originally published under the Creative Commons Attribution-NonCommercial-NoDerivatives license. It should have been published under the Creative Commons Attribution license. The license has been changed in the article online.

  • Access to Document (DOI)

• 実験近視の分子メカニズム

  栗原俊英

  新篇眼科プラクティス20 近視トータルマネジメント 生涯良好な視機能を保つために    93 - 95 2025.10

  Lead author, Last author, Corresponding author

• 光遺伝学を用いた網膜色素変性に対する視覚再生遺伝子治療

  栗原俊英

  月刊 『視覚障害』 448   10 - 14 2025.08

  Lead author, Last author, Corresponding author

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Presentations 【 Display / hide 】

Presentations 【 Display / hide 】

• Pathogenic mobile element insertions as overlooked causes of unresolved rare disease: ancestry-enriched founder alleles

  Takanobu Inoue, Hisato Suzuki, Daisuke Nakato, Shohei Kojima, Mie Inaba, Toshihide Kurihara, Naoya Morisada, Fuyuki Miya, Kenjiro Kosaki

  日本人類遺伝学会第71回大会, 

  2026.11

• Pathogenic mobile element insertions as overlooked causes of unresolved rare disease: clinical detection and ancestry-enriched founder alleles

  Yuka Nakano, Hisato Suzuki, Yukiko Kuroda, Hiroshi Yoshihashi, Nobuhiko Okamoto, Akane Kondo, Rika Kosaki, Kenichi Kashimada, Toshihide Kurihara, Meow-Keong Thong, Sok-Kun Tae, Mazlan Rifhan, Takashi Enokizono, Hiroshi Suzumura, Takeshi Yoshida, Shinji Kosugi, Seiji Mizuno, Mie Inaba, Natsuki Nakamura, Mayumi Matsufuji, Eri Ogawa, Hitomi Yagi, Mamiko Yamada, Emi Qian, Daisuke Nakato, Toshiki Takenouchi, Kenjiro Kosaki, Fuyuki Miya

  ASHG 2026 Annual Meeting, 

  2026.10

• オプトジェネティクス技術を用いた視覚再生遺伝子治療の研究開発

  栗原俊英

  第27回日本ロービジョン学会学術総会 ランチョンセミナー3, 

  2026.09

• 網膜・網膜色素上皮細胞・脈絡膜・強膜の眼科疾患病態形成における寄与と治療アプローチ

  栗原俊英

  アステラス製薬株式会社つくば研究センター「Tsukuba Seminar」, 

  2026.09

• 近視児童における2種類の光学式眼軸長測定装置による眼パラメータ測定値の比較

  金子歩駒, 重野雄太, 倉持美穂, 山内脩平, 大森朋子, 四倉絵里沙, 栗原俊英, 鳥居秀成, 根岸一乃

  第62回日本眼光学学会総会, 

  2026.08

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Research Projects of Competitive Funds, etc. 【 Display / hide 】

Research Projects of Competitive Funds, etc. 【 Display / hide 】

• Establishment of therapeutic intervention methods for fibrotic scar formation in age-related macular degeneration through hypoxia response control

  2024.04

  -

  2027.03

  基盤研究(C), Principal investigator

• 非視覚型光受容体による光マルチセンシング機構の解明と光新規治療法開発

  2022.10

  -

  2028.03

  国立研究開発法人日本医療研究開発機構(AMED), 令和4年度 「革新的先端研究開発支援事業（AMED-CREST）」, No Setting

• 低酸素応答制御機能を持つ静岡県産魚類由来成分の探索と疾患制御に関する研究

  2022.08

  -

  2025.03

  静岡県, マリンバイオテクノロジーを核としたシーズ創出研究業務委託 ￥286,800,000-, No Setting

• 低酸素応答を標的とした予防から治療までを網羅する網膜疾患制御技術開発

  2018.04

  -

  2021.03

  MEXT,JSPS, Grant-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (C), Principal investigator

• Approach for retinal diseases based on regulation of hypoxia response

  2015.04

  -

  2018.03

  MEXT,JSPS, Grant-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (C), Principal investigator

Intellectual Property Rights, etc. 【 Display / hide 】

Intellectual Property Rights, etc. 【 Display / hide 】

• クロセチンを含む組成物

  Date applied： 特願2026-008966  2026.01 

  Date issued： 特許第7896832号  2026.07

  Date registered： 2026.07

  Patent

• 脈絡膜の再建率の高い細胞移植法および細胞作成法

  Date applied： 特願2024-202214  2024.11 

  Date published： WO2026110832  2026.05 

  Patent

• 近視を予防または治療するための方法および組成物

  Date applied： 特願2024-103695  2024.06 

  Date announced： 特開2025-73060  2025.05 

  Patent

• α１ブロッカーを含む近視進行抑制用点眼剤

  Date applied： 特願2024-519839  2022.08 

  Date published： WO2024/048750  2024.03 

  Date issued： 特許第7640163号  2025.03

  Date registered： 2025.02

  Patent

• ＨＩＦ抑制用組成物

  Date applied： 特願2021-504090  2020.03 

  Date issued： 特許第7598591号  2024.12

  Date registered： 2024.12

  Patent

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Awards 【 Display / hide 】

Awards 【 Display / hide 】

• 第46回日本光医学・光生物学会学術奨励賞（医学領域）

  栗原俊英, 2024.07, 日本光医学・光生物学会, 非視覚光受容による近視進行抑制に関わる脳内回路の探索

• 日本眼科学会評議員会賞

  栗原俊英, 2024.04, 日本眼科学会, 光生物学を基盤とした眼疾患病態生理の理解と治療開発

• 第62回日本網膜硝子体学会総会優秀演題

  Ayaka Naka, Deokho Lee, Yan Zhang, Chiho Shoda, Satoshi Imanishi, Hiroyuki Nakashizuka, Satoru Yamagami, Kazuno Negishi, Akiharu Kubo, Toshihide Kurihara, 2023.11, 日本網膜硝子体学会, Claudin-1 deficiency in RPE leads to age-related retinal degeneration in mic

• The Keio Medical Science Rising Star Award

  Toshihide Kurihara, 2023.01, Keio University, Exploring the pathophysiology of the retina and myopia based on photobiology and the clinical adaptation

• 第72回日本臨床眼科学会学術展示優秀賞

  栗原俊英, 2019.04, 日本眼科学会, 白内障手術患者を対象とした血漿-房水グルコース濃度相関の血糖変動状態による変化

  　View Description

  第123回日本眼科学会総会

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Courses Taught 【 Display / hide 】

Courses Taught 【 Display / hide 】

• LECTURE SERIES, OPHTHALMOLOGY

  2026

Media Coverage 【 Display / hide 】

Media Coverage 【 Display / hide 】

• 脳研究の革命 ノーベル賞 網膜色素変性症の薬に応用

  信濃毎日新聞株式会社, 信濃毎日新聞, 2026.10

• （扉）光遺伝学、視覚再生へ進む治験 狙った細胞を操作、脳への実用化には課題も

  朝日新聞社, 朝日新聞 (朝日新聞デジタル) , 2025.11

• （扉）遺伝子治療、がんや希少疾患に 患者に合わせ、「土台」応用し費用・期間省く

  朝日新聞社, 朝日新聞 (朝日新聞デジタル) , 2025.10

  　View Summary

  体の細胞の遺伝子操作をする「遺伝子治療」。国内初の実施から３０年たち、多様な治療法が開発され、対象となる病気の種類も増えた。高額な開発費を抑える方法が模索されている。

• 光遺伝学を活用し、目の難病の視覚再生目指す 慶大など国内初の治験を開始

  サイエンスポータル, 国立研究開発法人 科学技術振興機構, 2025.03

  　View Summary

  神経細胞などの働きを光で制御する「光遺伝学」の手法を活用し、目の難病「網膜色素変性症」で失われた視覚の再生を目指す遺伝子治療薬の臨床試験（治験）を始めた、と慶應義塾大学と名古屋工業大学の共同研究グループが発表した。光遺伝学の臨床応用は国内初という。
  この目の難病は目の内側を覆い、光を受け取って神経の信号に変える働きをする網膜の視細胞が最初に障害を起こし、徐々に機能を失う進行性の失明難病。通常4000人から8000人に1人発症し、根本的な治療法は確立していない。世界の患者は200万人以上とされる。
  慶應大学医学部眼科学教室の栗原俊英准教授らの研究グループは、名古屋工業大学の神取秀樹教授らが開発した「キメラロドプシン」という光に対する感度が高い独自のタンパク質を使い、光遺伝学の手法を応用することで視覚再生効果と視細胞の保護効果があることをマウスで確認し、研究成果を2023年10月に発表していた。
  この成果を生かして慶應大学発のスタートアップ企業「レストアビジョン」（東京都港区）がキメラロドプシンの遺伝子治療薬（視覚再生治療製剤）「RV-001」を開発。栗原准教授らの研究グループは今回、既に視細胞の機能が失われた重症患者1人に対しRV-001を目に注射して1例目の投与を終えた。
  網膜にある双極細胞と呼ばれる神経細胞にキメラロドプシンを作る遺伝子を届け、視細胞の代わりに光の検知を担わせるのが目的。研究グループによると、これまで重い合併症などはないが、今後半年間経過を観察して安全性や有効性を確認する。今後6～15人を対象に治験を続ける予定だ。
  栗原准教授らの研究グループは「（治験を始めたRV-001は）視覚再生治療薬として世界初の実用化を目指す試みで、失明疾患に対する新たな治療法を提供する重要な一歩と位置付けられる」としている。
  光遺伝学は米スタンフォード大学のカール・ダイセロス教授が2005年に技術を確立した。脳研究に大きく貢献し、米国の医学賞であるラスカー賞（基礎分野）の20年授賞者に選ばれ、ノーベル賞の有力候補とされる。
  理化学研究所・脳科学総合研究センターの利根川進センター長（当時）らは2015年に「光遺伝学によってマウスのうつ状態を改善した」と発表した。現在はうつ病や睡眠障害、依存症など精神疾患の仕組みや臓器の働きの制御を研究する分野で活用されている。

• すんどめ ～網膜色素変性症と生きる〜

  名古屋テレビ放送・テレビ朝日系列全国24社, テレメンタリー2024, 2024.11

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  "すんどめ"の新競技で全国制覇へ！「今を楽しむことが一番」難病がある高校生ボクサーと全盲のシングルマザー 遺伝性のある網膜色素変性症、研究の最前線は
  
  愛知県岡崎市の石川凌久さんは、“当てないスパーリング”とも呼ばれるマスボクシングに打ち込む高校２年生。母親の智美さんは、２０代で網膜色素変性症という難病で失明した。凌久さんは、高校に入って”殴り合い”がある通常のボクシングをやりたいと思っていたが、受けて失明するのではないかと心配する智美さんの猛反対にあいマスボクシングを選んだ。網膜色素変性症は遺伝する可能性がある。視覚障がい者の選択に光を当てる。
  ナレーター：島貫凌アナウンサー
  名古屋テレビ放送
  
  https://www.tv-asahi.co.jp/telementary/backnumber/0257/

Memberships in Academic Societies 【 Display / hide 】

Memberships in Academic Societies 【 Display / hide 】

• Japan Society of Gene and Cell Therapy, 

  2026.04

  -

  Present

• The Japanese Society for Clinical Electrophysiology of Vision (JSCEV), 

  2026.01

  -

  Present

• The Macular Society, 

  2025.10

  -

  Present

• Japan Society for Ocular Circulation, 

  2025.04

  -

  Present

• The Japanese Society for Photomedicine and Photobiology, 

  2023.05

  -

  Present

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Committee Experiences 【 Display / hide 】

Committee Experiences 【 Display / hide 】

• 2022.11

  -

  Present

  Associate Editor for Neurodegeneration, Frontiers in Neuroscience

• 2022.10

  -

  Present

  眼科 外来医長, 慶應義塾大学病院