肥満による神経炎症と神経変性における代謝性炎症と体と脳の相互作用の媒介者としてのTNF

Chih Hung Lo¹, Jialiu Zeng²

¹Department of Biology, Syracuse University, Syracuse, NY 13244, USA; Interdisciplinary Neuroscience Program, Syracuse University, Syracuse, NY 13244, USA.

Ageing research reviews

|September 5, 2025

まとめ

肥満は腫瘍死因 (TNF) の放出を引き起こし,体と脳に炎症を引き起こします. TNF/TNFR1シグナリングをターゲットにすることで,肥満に関連する代謝および神経疾患の治療が可能になります.

科学分野:

神経免疫学
代謝障害
肥満に関する研究

背景:

体と脳の相互作用 (BBI) は,外周臓器の健康と神経機能の関係を結びます.
肥満のような代謝障害は神経学的疾患と併発しています
腫瘍死因 (TNF) は肥満に関連する炎症の重要な媒介です.

研究の目的:

肥満におけるTNF/TNFR1のシグナル伝達が脳を含む臓器システムにおけるホメオスタシスを破壊する方法を検討する.
代謝性炎症と神経炎症におけるTNFの役割を調査する.
肥満に関連する併発症に対するBBI軸内の治療目標の特定

主な方法:

TNF/TNFR1シグナル伝達経路に焦点を当てた文献レビュー
外周代謝機能障害 (脂肪細胞,肝細胞) のTNFの役割の分析
TNFが血脳障壁の浸透性と神経炎症に及ぼす影響の検討

主要な成果:

肥満に起因するTNF過剰生産は,外周インスリン抵抗性および代謝機能障害を引き起こす.
TNFが上昇すると血脳障壁の浸透性が増加し神経炎症が促進されます
脳内ではTNFはニューロンのインスリン信号伝達を阻害し,酸化ストレスを誘発し,神経変性を引き起こす.

結論:

TNF/TNFR1シグナリングは肥満,代謝機能障害,神経変性との間の重要なリンクです.
TNF/TNFR1シグナリングを調節することは,肥満に関連する併発症に対する有望な治療戦略です.
身体と脳の関係や細胞特有のメカニズムに関するさらなる研究が必要である.

キーワード:

TNFR1シグナリング血脳障壁 (BBB) の透過性身体と脳の相互作用メタボリック炎症ネクロプトーシス治療対象化

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