<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="GEO" alias="GSE104141" accession="SRP118629">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP118629</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA411796</EXTERNAL_ID>
      <EXTERNAL_ID namespace="GEO">GSE104141</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>Cranial pericytes derived from neural crest cells reveal an inherent cell type-specific defect in Alzheimer''s Disease</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Transcriptome Analysis"/>
      <STUDY_ABSTRACT>Forebrain microvasculature is defective in Alzheimer''s disease. To model the role of cranial pericytes in influencing endothelial cell functions, we developed a method for cranial-pericyte derivation from iPSCs. Our studies reveal inherent defects in cranial pericytes from familial AD iPSC. We also demonstrate a similar pathophysiology in perimary pericytes isolated from sporadic AD patients that can be rescued. Overall design: Comparison of primary and in vitro derived pericytes, as well as fAD and sAD versus control pericytes</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>GSE104141</CENTER_PROJECT_NAME>
    </DESCRIPTOR>
  </STUDY>
</STUDY_SET>
