Arzuhan Cetindag Ciltas , Sebahattin Karabulut , Bilal Sahin , Ahmet Kemal Filiz , Fatih Yulak , Mustafa Ozkaraca , Ozhan Karatas , Ali Cetin
{"title":"FGF-18 alleviates memory impairments and neuropathological changes in a rat model of Alzheimer's disease","authors":"Arzuhan Cetindag Ciltas , Sebahattin Karabulut , Bilal Sahin , Ahmet Kemal Filiz , Fatih Yulak , Mustafa Ozkaraca , Ozhan Karatas , Ali Cetin","doi":"10.1016/j.npep.2023.102367","DOIUrl":null,"url":null,"abstract":"<div><p><span><span>Alzheimer's disease (AD) is a multifactorial pathology marked by </span>amyloid beta<span><span> (Aβ) accumulation, tau hyperphosphorylation, and progressive cognitive decline. Previous studies show that </span>fibroblast growth factor 18<span> (FGF18) exerts a neuroprotective<span> effect in experimental models of neurodegeneration; however, how it affects AD pathology remains unknown. This study aimed to ascertain the impact of FGF18 on the behavioral and neuropathological changes in the rat model of sporadic AD induced by intracerebroventricular (ICV) injection of </span></span></span></span>streptozotocin<span><span> (STZ). The rats were treated with FGF18 (0.94 and 1.88 pmol, ICV) on the 15th day after STZ injection. Their cognitive function was assessed in the Morris water maze and </span>passive avoidance<span><span><span> tests for 5 days from the 16th to the 21st days. Aβ levels and histological signs of neurotoxicity were detected using the enzyme-linked immunosorbent assay (ELISA) assay and histopathological analysis of the brain, respectively. FGF18 mildly ameliorated the STZ-induced </span>cognitive impairment; the Aβ accumulation was reduced; and the neuronal damage including </span>pyknosis<span> and apoptosis was alleviated in the rat brain. This study highlights the promising therapeutic potential for FGF18 in managing AD.</span></span></span></p></div>","PeriodicalId":2,"journal":{"name":"ACS Applied Bio Materials","volume":null,"pages":null},"PeriodicalIF":4.6000,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Bio Materials","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0143417923000483","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MATERIALS SCIENCE, BIOMATERIALS","Score":null,"Total":0}
引用次数: 0
Abstract
Alzheimer's disease (AD) is a multifactorial pathology marked by amyloid beta (Aβ) accumulation, tau hyperphosphorylation, and progressive cognitive decline. Previous studies show that fibroblast growth factor 18 (FGF18) exerts a neuroprotective effect in experimental models of neurodegeneration; however, how it affects AD pathology remains unknown. This study aimed to ascertain the impact of FGF18 on the behavioral and neuropathological changes in the rat model of sporadic AD induced by intracerebroventricular (ICV) injection of streptozotocin (STZ). The rats were treated with FGF18 (0.94 and 1.88 pmol, ICV) on the 15th day after STZ injection. Their cognitive function was assessed in the Morris water maze and passive avoidance tests for 5 days from the 16th to the 21st days. Aβ levels and histological signs of neurotoxicity were detected using the enzyme-linked immunosorbent assay (ELISA) assay and histopathological analysis of the brain, respectively. FGF18 mildly ameliorated the STZ-induced cognitive impairment; the Aβ accumulation was reduced; and the neuronal damage including pyknosis and apoptosis was alleviated in the rat brain. This study highlights the promising therapeutic potential for FGF18 in managing AD.
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