老化システム環境は,神経生成と認知機能を否定的に調節する
Saul A Villeda1, Jian Luo, Kira I Mosher
1Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, USA.
Nature
|September 3, 2011
まとめ
老化は脳幹細胞の活動と記憶を損なう. 年老いたマウスの血液因子は,若いマウスの神経生成と認知機能を低下させ,CCL11を重要な分子として特定します. これは,血液を媒介する要因が,年齢に関連する認知機能低下に寄与することを示唆しています.
科学分野:
- 神経科学は神経科学である.
- 老化に関する研究
- 幹細胞生物学 幹細胞生物学
背景:
- 老化は,神経幹細胞/原始細胞の減少と,中枢神経系における神経生成につながります.
- 認知機能は年齢とともに低下しますが,運動などの要因によって改善することができます.
- 年齢に関連した神経生成の衰退における全身的要因の役割は完全に理解されていません.
研究 の 目的:
- 成人のニューロゲネシスと認知機能に対する全身的,血液媒介の要因の影響を,年齢に依存した方法で調査する.
- 血中の特定の分子を特定し,老化中の神経生成と学習に影響を与える.
主な方法:
- ネズミのヘテロクロニックパラバイオシスで,若いと古いシステム環境の影響を研究する.
- シナプス可塑性,文脈的な恐怖条件付け,空間的学習と記憶の評価.
- 血および脳脊髄液のケモカインレベル,特にCCL11 (エオタキシン) の測定.
- 若いマウスのCCL11レベルをin vivoで操作する.
主要な成果:
- 古いシステム環境や古いマウスプラズマへの曝露は,若いマウスのニューロゲネシス,シナプス可塑性,認知能力を低下させた.
- ケモカインCCL11のプラズマ濃度は,パラビオンと老いたマウスの神経生成の低下と相関していた.
- CCL11レベルは,健康な高齢者の血と脳脊髄液で上昇した.
- 若いマウスの外周CCL11の増加は,神経生成の減少と学習と記憶の障害を引き起こしました.
結論:
- 系統的環境における血液媒介の要因は,年齢に依存した方法で成人の神経生成を阻害することがあります.
- ケモカインCCL11は,年齢に関連した神経生成と認知機能の低下に貢献する血液媒介の重要な要因として特定されています.
- これらの発見は,血液を媒介する要因を標的とした治療が,年齢に関連する認知障害の治療戦略を提供することを示唆しています.
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