Catur Kusumo, Muhammad Arifin Parenrengi, Wihasto Suryaningtyas, Achmad Fahmi, Budi Utomo, I Ketut Sudiana
{"title":"Aquaporin-9 as a biomarker for hydrocephalus: Insights from experimental rat models.","authors":"Catur Kusumo, Muhammad Arifin Parenrengi, Wihasto Suryaningtyas, Achmad Fahmi, Budi Utomo, I Ketut Sudiana","doi":"10.25259/SNI_1024_2024","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Hydrocephalus, characterized by ventricular enlargement often associated with elevated intracranial pressure, necessitates reliable biomarkers for accurate diagnosis. Aquaporin-9 (AQP-9), localized at the interface of cerebrospinal fluid (CSF) spaces and blood vessels, plays a critical role in brain water homeostasis but remains underexplored in the context of hydrocephalus. Further investigation into AQP-9 expression in CSF is essential to elucidate its potential as a diagnostic biomarker and its role in hydrocephalus pathophysiology.</p><p><strong>Methods: </strong>This experimental study utilized 10-12-week-old Sprague-Dawley rats (<i>Rattus norvegicus</i>) weighing 200-250 g, randomly assigned to three groups. CSF served as the primary unit of analysis. AQP-9 levels were quantified using the enzyme-linked immunosorbent assay Sandwich method, with CSF sampling conducted at 7-day intervals over 21 days.</p><p><strong>Results: </strong>AQP-9 levels were significantly elevated in hydrocephalic mice compared to controls, with the highest levels on day 21 (887.62 ± 88.72). CSF drainage resulted in a notable reduction in AQP-9 levels at all time points. Statistical analysis confirmed significant differences across groups (<i>P</i> < 0.05), with <i>post hoc</i> tests showing meaningful reductions in AQP-9 levels after drainage compared to hydrocephalic states. These findings suggest AQP-9 as a potential biomarker for hydrocephalus diagnosis and monitoring therapeutic response.</p><p><strong>Conclusion: </strong>AQP-9 shows promise as a biomarker for hydrocephalus, with levels reflecting disease progression and decreasing after CSF drainage. This highlights its potential for diagnosis and therapeutic monitoring, warranting further validation.</p>","PeriodicalId":94217,"journal":{"name":"Surgical neurology international","volume":"16 ","pages":"58"},"PeriodicalIF":0.0000,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11878738/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Surgical neurology international","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.25259/SNI_1024_2024","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Hydrocephalus, characterized by ventricular enlargement often associated with elevated intracranial pressure, necessitates reliable biomarkers for accurate diagnosis. Aquaporin-9 (AQP-9), localized at the interface of cerebrospinal fluid (CSF) spaces and blood vessels, plays a critical role in brain water homeostasis but remains underexplored in the context of hydrocephalus. Further investigation into AQP-9 expression in CSF is essential to elucidate its potential as a diagnostic biomarker and its role in hydrocephalus pathophysiology.
Methods: This experimental study utilized 10-12-week-old Sprague-Dawley rats (Rattus norvegicus) weighing 200-250 g, randomly assigned to three groups. CSF served as the primary unit of analysis. AQP-9 levels were quantified using the enzyme-linked immunosorbent assay Sandwich method, with CSF sampling conducted at 7-day intervals over 21 days.
Results: AQP-9 levels were significantly elevated in hydrocephalic mice compared to controls, with the highest levels on day 21 (887.62 ± 88.72). CSF drainage resulted in a notable reduction in AQP-9 levels at all time points. Statistical analysis confirmed significant differences across groups (P < 0.05), with post hoc tests showing meaningful reductions in AQP-9 levels after drainage compared to hydrocephalic states. These findings suggest AQP-9 as a potential biomarker for hydrocephalus diagnosis and monitoring therapeutic response.
Conclusion: AQP-9 shows promise as a biomarker for hydrocephalus, with levels reflecting disease progression and decreasing after CSF drainage. This highlights its potential for diagnosis and therapeutic monitoring, warranting further validation.