• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

探讨 PPARγ 激动剂调节神经退行性疾病中记忆障碍的分子机制。

Exploring the molecular mechanisms of PPARγ agonists in modulating memory impairment in neurodegenerative disorders.

机构信息

Bio Environmental Health Hazards Research Center, Jiroft University of Medical Sciences, Jiroft, Iran.

Student Research Committee, Jiroft University of Medical Sciences, Jiroft, Iran.

出版信息

Mol Biol Rep. 2024 Aug 31;51(1):945. doi: 10.1007/s11033-024-09850-6.

DOI:10.1007/s11033-024-09850-6
PMID:39215798
Abstract

Neurodegenerative diseases are characterized by progressive memory impairment and cognitive decline. This review aims to unravel the molecular mechanisms involved in the enhancement of memory function and mitigation of memory impairment through the activation of PPARγ agonists in neurodegenerative diseases. The findings suggest that PPARγ agonists modulate various molecular pathways involved in memory formation and maintenance. Activation of PPARγ enhances synaptic plasticity, promotes neuroprotection, suppresses neuroinflammation, attenuates oxidative stress, and regulates amyloid-beta metabolism. The comprehensive understanding of these molecular mechanisms would facilitate the development of novel therapeutic approaches targeting PPARγ to improve memory function and ultimately to alleviate the burden of neurodegenerative diseases. Further research, including clinical trials, is warranted to explore the efficacy, safety, and optimal use of specific PPARγ agonists as potential therapeutic agents in the treatment of memory impairments associated with neurodegenerative diseases.

摘要

神经退行性疾病的特征是进行性记忆障碍和认知能力下降。本综述旨在揭示通过激活神经退行性疾病中的过氧化物酶体增殖物激活受体γ(PPARγ)激动剂来增强记忆功能和减轻记忆障碍的分子机制。研究结果表明,PPARγ 激动剂调节参与记忆形成和维持的各种分子途径。激活 PPARγ 可增强突触可塑性、促进神经保护、抑制神经炎症、减轻氧化应激和调节淀粉样蛋白-β代谢。全面了解这些分子机制将有助于开发针对 PPARγ 的新型治疗方法,以改善记忆功能,最终减轻神经退行性疾病的负担。需要进一步的研究,包括临床试验,以探索特定的 PPARγ 激动剂作为治疗与神经退行性疾病相关的记忆障碍的潜在治疗剂的疗效、安全性和最佳使用方法。

相似文献

1
Exploring the molecular mechanisms of PPARγ agonists in modulating memory impairment in neurodegenerative disorders.探讨 PPARγ 激动剂调节神经退行性疾病中记忆障碍的分子机制。
Mol Biol Rep. 2024 Aug 31;51(1):945. doi: 10.1007/s11033-024-09850-6.
2
Exploring the molecular mechanisms of curcumin in modulating memory impairment in neurodegenerative disorders.探索姜黄素调节神经退行性疾病记忆障碍的分子机制。
Mol Biol Rep. 2024 Dec 9;52(1):45. doi: 10.1007/s11033-024-10115-5.
3
Peroxisome proliferator-activated receptor gamma up-regulates the Bcl-2 anti-apoptotic protein in neurons and induces mitochondrial stabilization and protection against oxidative stress and apoptosis.过氧化物酶体增殖物激活受体γ上调神经元中的Bcl-2抗凋亡蛋白,并诱导线粒体稳定,保护其免受氧化应激和细胞凋亡的影响。
J Biol Chem. 2007 Dec 21;282(51):37006-15. doi: 10.1074/jbc.M700447200. Epub 2007 Oct 25.
4
Sesame oil mitigates memory impairment, oxidative stress, and neurodegeneration in a rat model of Alzheimer's disease. A pivotal role of NF-κB/p38MAPK/BDNF/PPAR-γ pathways.芝麻油可减轻阿尔茨海默病大鼠模型的记忆障碍、氧化应激和神经退行性变。NF-κB/p38MAPK/BDNF/PPAR-γ 通路发挥关键作用。
J Ethnopharmacol. 2021 Mar 1;267:113468. doi: 10.1016/j.jep.2020.113468. Epub 2020 Oct 10.
5
Modulation of the Nitrergic Pathway via Activation of PPAR-γ Contributes to the Neuroprotective Effect of Pioglitazone Against Streptozotocin-Induced Memory Dysfunction.通过激活过氧化物酶体增殖物激活受体γ调节一氧化氮能途径有助于吡格列酮对链脲佐菌素诱导的记忆功能障碍的神经保护作用。
J Mol Neurosci. 2015 Jul;56(3):739-50. doi: 10.1007/s12031-015-0508-7. Epub 2015 Feb 18.
6
Rosiglitazone rescues human neural stem cells from amyloid-beta induced ER stress via PPARγ dependent signaling.罗格列酮通过 PPARγ 依赖的信号通路拯救人神经干细胞免受淀粉样β诱导的内质网应激。
Exp Cell Res. 2018 Sep 15;370(2):312-321. doi: 10.1016/j.yexcr.2018.06.033. Epub 2018 Jun 28.
7
PPARγ agonists regulate bidirectional transport of amyloid-β across the blood-brain barrier and hippocampus plasticity in db/db mice.过氧化物酶体增殖物激活受体γ激动剂调节db/db小鼠中淀粉样β蛋白跨血脑屏障的双向转运及海马可塑性。
Br J Pharmacol. 2016 Jan;173(2):372-85. doi: 10.1111/bph.13378. Epub 2015 Dec 19.
8
Phytohormone Abscisic Acid Improves Memory Impairment and Reduces Neuroinflammation in 5xFAD Mice by Upregulation of LanC-Like Protein 2.植物激素脱落酸通过上调 LanC 样蛋白 2 改善 5xFAD 小鼠的记忆障碍并减少神经炎症。
Int J Mol Sci. 2020 Nov 10;21(22):8425. doi: 10.3390/ijms21228425.
9
PPARγ as a therapeutic target to rescue mitochondrial function in neurological disease.过氧化物酶体增殖物激活受体γ作为挽救神经疾病中线粒体功能的治疗靶点。
Free Radic Biol Med. 2016 Nov;100:153-163. doi: 10.1016/j.freeradbiomed.2016.06.023. Epub 2016 Jun 25.
10
Rosiglitazone synergizes the neuroprotective effects of valproic acid against quinolinic acid-induced neurotoxicity in rats: targeting PPARγ and HDAC pathways.罗格列酮增强丙戊酸对喹啉酸诱导的大鼠神经毒性的神经保护作用:靶向过氧化物酶体增殖物激活受体γ和组蛋白去乙酰化酶途径。
Neurotox Res. 2014 Aug;26(2):130-51. doi: 10.1007/s12640-014-9458-z. Epub 2014 Feb 25.

引用本文的文献

1
Ethanol-Induced Depression: Exploring the Underlying Molecular Mechanisms.乙醇诱导的抑郁:探索潜在的分子机制
Cell Mol Neurobiol. 2025 May 22;45(1):49. doi: 10.1007/s10571-025-01569-7.
2
The Role of Nutrition, Oxidative Stress, and Trace Elements in the Pathophysiology of Autism Spectrum Disorders.营养、氧化应激和微量元素在自闭症谱系障碍病理生理学中的作用
Int J Mol Sci. 2025 Jan 18;26(2):808. doi: 10.3390/ijms26020808.
3
Exploring the molecular mechanisms of curcumin in modulating memory impairment in neurodegenerative disorders.

本文引用的文献

1
Pioglitazone ameliorates DOX-induced cognitive impairment by mitigating inflammation, oxidative stress, and apoptosis of hippocampal neurons in rats.吡格列酮通过减轻大鼠海马神经元的炎症、氧化应激和凋亡改善 DOX 引起的认知障碍。
Behav Brain Res. 2024 Feb 4;457:114714. doi: 10.1016/j.bbr.2023.114714. Epub 2023 Oct 12.
2
Exploring Rosiglitazone's Potential to Treat Alzheimer's Disease through the Modulation of Brain-Derived Neurotrophic Factor.探索罗格列酮通过调节脑源性神经营养因子治疗阿尔茨海默病的潜力。
Biology (Basel). 2023 Jul 24;12(7):1042. doi: 10.3390/biology12071042.
3
The role of brain derived neurotrophic factor in central nervous system.
探索姜黄素调节神经退行性疾病记忆障碍的分子机制。
Mol Biol Rep. 2024 Dec 9;52(1):45. doi: 10.1007/s11033-024-10115-5.
脑源性神经营养因子在中枢神经系统中的作用。
Front Aging Neurosci. 2022 Sep 8;14:986443. doi: 10.3389/fnagi.2022.986443. eCollection 2022.
4
Regulation of Neuroinflammatory Signaling by PPARγ Agonist in Mouse Model of Diabetes.过氧化物酶体增殖物激活受体γ激动剂在糖尿病小鼠模型中对神经炎症信号的调节。
Int J Mol Sci. 2022 May 14;23(10):5502. doi: 10.3390/ijms23105502.
5
Structural LTP: Signal transduction, actin cytoskeleton reorganization, and membrane remodeling of dendritic spines.结构性长时程增强:树突棘的信号转导、肌动蛋白细胞骨架重组及膜重塑
Curr Opin Neurobiol. 2022 Jun;74:102534. doi: 10.1016/j.conb.2022.102534. Epub 2022 Apr 7.
6
Role of Nrf2 in Synaptic Plasticity and Memory in Alzheimer's Disease.Nrf2 在阿尔茨海默病中的突触可塑性和记忆中的作用。
Cells. 2021 Jul 25;10(8):1884. doi: 10.3390/cells10081884.
7
Molecular mechanism of hippocampal long-term potentiation - Towards multiscale understanding of learning and memory.海马体长期增强效应的分子机制——迈向对学习与记忆的多尺度理解
Neurosci Res. 2022 Feb;175:3-15. doi: 10.1016/j.neures.2021.08.001. Epub 2021 Aug 8.
8
Neuroprotective and antioxidative effects of pioglitazone in brain tissue adjacent to the ischemic core are mediated by PI3K/Akt and Nrf2/ARE pathways.吡格列酮通过 PI3K/Akt 和 Nrf2/ARE 通路对缺血核心区脑组织发挥神经保护和抗氧化作用。
J Mol Med (Berl). 2021 Aug;99(8):1073-1083. doi: 10.1007/s00109-021-02065-3. Epub 2021 Apr 16.
9
The Protective Effects of Peroxisome Proliferator-Activated Receptor Gamma in Cerebral Ischemia-Reperfusion Injury.过氧化物酶体增殖物激活受体γ在脑缺血再灌注损伤中的保护作用
Front Neurol. 2020 Nov 17;11:588516. doi: 10.3389/fneur.2020.588516. eCollection 2020.
10
Sesame oil mitigates memory impairment, oxidative stress, and neurodegeneration in a rat model of Alzheimer's disease. A pivotal role of NF-κB/p38MAPK/BDNF/PPAR-γ pathways.芝麻油可减轻阿尔茨海默病大鼠模型的记忆障碍、氧化应激和神经退行性变。NF-κB/p38MAPK/BDNF/PPAR-γ 通路发挥关键作用。
J Ethnopharmacol. 2021 Mar 1;267:113468. doi: 10.1016/j.jep.2020.113468. Epub 2020 Oct 10.