ABA Supplementation Rescues IRS2 and BDNF mRNA Levels in a Triple-Transgenic Mice Model of Alzheimer's Disease

被引:2
作者
Alves-Borba, Laryssa [1 ,2 ]
Espinosa-Fernandez, Veronica [1 ,2 ]
Canseco-Rodriguez, Ania [1 ,2 ]
Maria Sanchez-Perez, Ana [1 ,2 ]
机构
[1] Univ Jaume 1, Neurobiotecnol Grp, Fac Hlth Sci, Avda de Vicent Sos Baynat,S N, Castellon de La Plana 12071, Spain
[2] Univ Jaume 1, Inst Adv Mat INAM, Avda de Vicent Sos Baynat,S N, Castellon de La Plana 12071, Spain
关键词
Alzheimer's disease; hippocampus; insulin signal; neuroinflammation; neuroprotector; neurotrophic factor; phytohormones; IMPAIRED INSULIN; EXPRESSION; BRAIN; ALPHA; DEFICITS;
D O I
10.3233/ADR-230056
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Insulin resistance underlies Alzheimer's disease (AD) by affecting neuroinflammation and brain-derived neurotrophic factor (BDNF) expression. Here, we evaluated the effect of early and late-start abscisic acid (ABA) intervention on hippocampal BDNF, tumor necrosis factor alpha (TNF alpha), and insulin receptors substrates (IRS) 1/2 mRNA levels in a triple-transgenic mice model of AD. Transgenic mice displayed lower BDNF and IRS2, equal IRS1, and higher TNF alpha expression compared to wild-type mice. Late ABA treatment could rescue TNF alpha and increased IRS1/2 expression. However, early ABA administration was required to increase BDNF expression. Our data suggests that early intervention with ABA can prevent AD, via rescuing IRS1/2 and BDNF expression.
引用
收藏
页码:1007 / 1013
页数:7
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