研究課題/領域番号 |
23K19447
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研究種目 |
研究活動スタート支援
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配分区分 | 基金 |
審査区分 |
0802:生体の構造と機能およびその関連分野
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研究機関 | 富山大学 |
研究代表者 |
Karim Mariam 富山大学, 学術研究部医学系, 特命助教 (00984577)
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研究期間 (年度) |
2023-08-31 – 2025-03-31
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研究課題ステータス |
交付 (2023年度)
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配分額 *注記 |
2,860千円 (直接経費: 2,200千円、間接経費: 660千円)
2024年度: 1,430千円 (直接経費: 1,100千円、間接経費: 330千円)
2023年度: 1,430千円 (直接経費: 1,100千円、間接経費: 330千円)
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キーワード | Bone Formation / NAD+ metabolism / Bone Mineral density / Aging / Osteoporosis |
研究開始時の研究の概要 |
Nicotinamide adenine dinucleotide is a life essential coenzyme. NAD+ metabolism has significant role in age related pathologies. Osteoporosis is geriatric disorder with unknown cause in relation to NAD+ metabolism. The goal is to establish therapeutics for osteoporosis using NAD+ boosting therapies.
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研究実績の概要 |
NAD+ depleted mice model was used to study bones, in which Denovo and Preiss handler pathways of NAD biosynthesis are ablated. I found NAD+ depletion cause abnormal faulty bone growth. Upon morphometrics bone showed high bone resorptive cell known as osteoclast. MicroCT analysis these mice showed low Bone mineral density which is clinical sign for osteoporosis. Hence, it is established that NAD+ levels at young age is crucial for maintaining bone health. Research presented in following conferences: 1.Karim M, Nakagawa T. NAD+ level at a young age affects skeletal muscle functions at an old age. 日本トリフ-12442;トファン研究会 第42回学術集会; 2023 Dec 2-3; 富山. 2.Karim M, Nakagawa T. NAD+ level at a young age affects skeletal muscle functions at an old age.第97回日本薬理学会年会; 2023 Dec 14-16; Kobe.
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現在までの達成度 (区分) |
現在までの達成度 (区分)
3: やや遅れている
理由
Mice models were studied, and new finding are indicative towards the more specific Bone cell specific deletion. To elucidate the role of osteoclast specific NAD depletion. More mice models are in making process consuming slightly more time. Moreover, this study aims to study old mice of 24months, which also extended the study time period.
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今後の研究の推進方策 |
For this promising study next, I would like to examine bones of Osteoclast specific NAD+ depleted mice. Along with the bone I will check the interplay of lipid and amino acid metabolism in maintaining bone NAD+ homeostasis. Histo morphometric analysis of old age mice will be considered. The plan is to establish therapeutics for osteoporosis targeting NAD+ boosting therapies.
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