Silent Information Regulator T1 in Aqueous Humor of Patients with Age-Related Macular Degeneration

Tatsuya Mimura1, 2, *, Hideharu Funatsu3, Hidetaka Noma4, Aki Kondo2, Atsushi Mizota1
1 Department of Ophthalmology, School of Medicine, Teikyo University, Tokyo, Japan
2 Department of Ophthalmology, Tokyo Women's Medical University Medical Center East, Tokyo, Japan
3 Department of Ophthalmology, Yachiyo Medical Center, Tokyo Women’s Medical University, Chiba, Japan
4 Department of Ophthalmology, Hachioji Medical Center, Tokyo Medical University, Tokyo, Japan

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© 2021 Mimura et al.

open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

* Address correspondence to this author at the Department of Ophthalmology, School of Medicine, Teikyo University, 2-11-1 Kaga, Itabashi-ku, Tokyo, 173-8605 Japan; Tel: +81-3-3964-1211, Fax: +81-3-3964-1402; E-mail:



The purpose of this study is to compare the aqueous humor level of Silent Information Regulator T1 (SIRT1) between patients with Age-related Macular Degeneration (AMD) and cataract patients.

Materials and Methods:

Aqueous humor level of SIRT1 was measured by enzyme-linked immunosorbent assay in 13 patients with wet-type AMD (n=13, AMD group) and 13 patients with cataracts (cataract group). In addition, the thickness of each retinal layer was determined by optical coherence tomography.


The aqueous humor level of SIRT1 was significantly lower in the AMD group than in the cataract group (p=0.007). In the AMD group, the SIRT1 level was positively correlated with the thickness of the retinal ganglion cell layer (r=0.31) and the inner nuclear layer (r=0.76).


The aqueous level of SIRT1 decreased as the ganglion cell layer and inner nuclear layer became thinner, suggesting that reduction of SIRT1 activity might be involved in the pathogenesis of this disease.

Keywords: Age-related macular degeneration, Aqueous humor, Silent information regulator T1, Ganglion, Cell, Cataract patients, Optic neuritis.