Assessment of suberoylanilide hydroxamic acid on a Alzheimer?s disease model induced by ?-amyloid(1-42) in aged female mice: Neuromodulatory and epigenetic effect

被引：8

作者：

Rocha, Kellen Mariane Athaide ^{[1
]}

Machado, Franciele Romero ^{[1
]}

Giacomeli, Renata ^{[1
]}

Boeira, Silvana Peterini ^{[1
]}

Jesse, Cristiano Ricardo ^{[1
]}

de Gomes, Marcelo Gomes ^{[1
,2
]}

机构：

[1] Fed Univ Pampa, Lab Pharmacol & Toxicol Evaluat Appl Bioact Mol, BR-97650000 Itaqui, RS, Brazil

[2] Fed Univ Pampa, Lab Pharmacol, Toxicol Evaluat Appl Bioact Mol, LaftamBio Pampa, Campus Itaqui, BR-97650000 Itaqui, RS, Brazil

来源：

CHEMICO-BIOLOGICAL INTERACTIONS | 2023年 / 375卷

关键词：

Alzheimer?s disease; Epigenetic; Memory; HDAC; SAHA; HISTONE DEACETYLASES ACTIVITIES; AMYLOID-BETA; NEUROTROPHIC FACTOR; GENE-TRANSCRIPTION; MOUSE MODEL; BDNF; MEMORY; CREB; EXERCISE; ACETYLTRANSFERASES;

D O I：

10.1016/j.cbi.2023.110429

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Alzheimer's disease (AD) is a neurodegenerative disease that affects several elderly people per years. AD is a pathology of multifactorial etiology, resulting from multiple environmental and genetic determinants. However, there is no effective pharmacological alternative for the treatment of this illness. In this sense, the purpose of current study was to characterize the mechanisms by which A beta 1-42 injection via intracerebroventricular induces neurobehavioral changes in a time-course curve. In addition, suberoylanilide hydroxamic acid (SAHA) inhibitor of histone deacetylase (HDAC) was used to investigate the involvement of epigenetic modifications A beta 1-42-caused in aged female mice. In general manner, A beta 1-42 injection induced a major neurochemical disturbance in hippocampus and prefrontal cortex of animals and a serious impairment of memory. Overall, SAHA treatment attenuated neurobehavioral changes caused by A beta 1-42 injection in aged female mice. The subchronic effects presented of SAHA were through modulation of HDAC activity, regulation of brain-derived neurotrophic factor (BDNF) levels and expression of BDNF mRNA, accompanied by unlocking cAMP/PKA/pCREB pathway in hippocampus and prefrontal cortex of animals.

引用

页数：11

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