Arunima Kapoor , Shubir Dutt , Amy Nguyen , Trevor Lohman , Aimée Gaubert , John Paul M. Alitin , Isabel J Sible , Anisa Marshall , Fatemah Shenasa , Allison C Engstrom , David Robert Bradford , Kathleen Rodgers , Daniel A Nation
{"title":"Endothelial progenitor cells and cerebral small vessel disease in APOE4 carriers","authors":"Arunima Kapoor , Shubir Dutt , Amy Nguyen , Trevor Lohman , Aimée Gaubert , John Paul M. Alitin , Isabel J Sible , Anisa Marshall , Fatemah Shenasa , Allison C Engstrom , David Robert Bradford , Kathleen Rodgers , Daniel A Nation","doi":"10.1016/j.cccb.2025.100378","DOIUrl":null,"url":null,"abstract":"<div><div><em>APOE4</em> carriers at genetic risk for Alzheimer's disease exhibit early cerebrovascular dysfunction, which may be triggered by endothelial dysfunction. Endothelial progenitor cells (EPCs) represent cell populations involved in promoting angiogenesis and facilitating vascular repair in response to injury. We examined whether elevated EPCs are associated with lower cerebral small vessel disease burden in <em>APOE4</em> carriers prior to cognitive decline. Independently living older adults (<em>N</em> = 109, mean age = 70.5 years; SD = 7.9; 34.9 % male) free of dementia or clinical stroke underwent brain MRI and venipuncture. Small vessel disease was determined using a validated scale. White matter hyperintensity (WMH) volume was determined using the lesion segmentation toolbox. PBMCs were cultured and EPCs were defined as number of colony forming units in vitro. Regression analysis revealed an association between average number of EPC colonies and lower small vessel disease load (<em>p</em> = .026) and WMH volume (<em>p</em> = .002), in <em>APOE4</em> carriers. Findings suggest that EPC colony count may indicate activation of mechanisms which protect cerebrovascular function in <em>APOE4</em> carriers prior to the development of cognitive decline.</div></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"8 ","pages":"Article 100378"},"PeriodicalIF":1.9000,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cerebral circulation - cognition and behavior","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2666245025000029","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
APOE4 carriers at genetic risk for Alzheimer's disease exhibit early cerebrovascular dysfunction, which may be triggered by endothelial dysfunction. Endothelial progenitor cells (EPCs) represent cell populations involved in promoting angiogenesis and facilitating vascular repair in response to injury. We examined whether elevated EPCs are associated with lower cerebral small vessel disease burden in APOE4 carriers prior to cognitive decline. Independently living older adults (N = 109, mean age = 70.5 years; SD = 7.9; 34.9 % male) free of dementia or clinical stroke underwent brain MRI and venipuncture. Small vessel disease was determined using a validated scale. White matter hyperintensity (WMH) volume was determined using the lesion segmentation toolbox. PBMCs were cultured and EPCs were defined as number of colony forming units in vitro. Regression analysis revealed an association between average number of EPC colonies and lower small vessel disease load (p = .026) and WMH volume (p = .002), in APOE4 carriers. Findings suggest that EPC colony count may indicate activation of mechanisms which protect cerebrovascular function in APOE4 carriers prior to the development of cognitive decline.