{"title":"Intranasal Aβ<sub>1-42</sub> Exposure Led To Neurobehavioral Alteration, Neuroinflammatory and Neurodegenerative Molecular Biomarkers in Mice Brain.","authors":"Avtar Singh Gautam, Mohammad Zunaid Akhtar, Lasure Vaibhav Uttamrao, Nisha Kumari, Shivam Kumar Pandey, Mangaldeep Dey, Rakesh Kumar Singh","doi":"10.1007/s11481-025-10246-x","DOIUrl":null,"url":null,"abstract":"<p><p>In this study, we aimed to evaluate the AD structural hallmarks along with brain biomarkers and neurobehavioral alterations in a repeated intranasal Aβ<sub>1-42</sub> exposure mouse model. This model is a simple, non-invasive, and less stressful method and may allow direct access of Aβ to the brain. The results of this study showed a dose-dependent increase in the level of Aβ<sub>1-42</sub> deposition, tau phosphorylation, neuroinflammatory and oxidative stress biomarkers in brain tissue, along with learning and memory deficits in mice. This model may be suitable for evaluating the biochemical, structural, functional histological alterations, along with the neurobehavioral deficits mimicking AD.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"20 1","pages":"83"},"PeriodicalIF":3.5000,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/s11481-025-10246-x","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
In this study, we aimed to evaluate the AD structural hallmarks along with brain biomarkers and neurobehavioral alterations in a repeated intranasal Aβ1-42 exposure mouse model. This model is a simple, non-invasive, and less stressful method and may allow direct access of Aβ to the brain. The results of this study showed a dose-dependent increase in the level of Aβ1-42 deposition, tau phosphorylation, neuroinflammatory and oxidative stress biomarkers in brain tissue, along with learning and memory deficits in mice. This model may be suitable for evaluating the biochemical, structural, functional histological alterations, along with the neurobehavioral deficits mimicking AD.