<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>43(5)</volume><submitter>Chai YL</submitter><pubmed_abstract>Chronic cerebral hypoperfusion (CCH) is postulated to underlie multiple pathophysiological processes in vascular dementia (VaD), including extracellular matrix dysfunction. While several extracellular matrix proteins, namely cyclophilin A (CypA), extracellular matrix metalloproteinase inducer (EMMPRIN) and gelatinases (matrix metalloproteinases, MMP-2 and -9) have been investigated in acute stroke, their involvement in CCH and VaD remains unclear. In this study, CypA-EMMPRIN-gelatinase proteins were analysed in a clinical cohort of 36 aged, cognitively unimpaired subjects and 48 VaD patients, as well as in a bilateral carotid artery stenosis mouse model of CCH. Lower CypA and higher EMMPRIN levels were found in both VaD serum and CCH mouse brain. Furthermore, gelatinases were differentiall</pubmed_abstract><journal>Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism</journal><pagination>722-735</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10108186</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Chronic cerebral hypoperfusion alters the CypA-EMMPRIN-gelatinase pathway: Implications for vascular dementia.</pubmed_title><pmcid>PMC10108186</pmcid><pubmed_authors>Selvaraji S</pubmed_authors><pubmed_authors>Koo EH</pubmed_authors><pubmed_authors>Hilal S</pubmed_authors><pubmed_authors>Chen CP</pubmed_authors><pubmed_authors>Chai YL</pubmed_authors><pubmed_authors>Arumugam TV</pubmed_authors><pubmed_authors>Jo DG</pubmed_authors><pubmed_authors>Rajeev V</pubmed_authors><pubmed_authors>Lai MK</pubmed_authors><pubmed_authors>Poh L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Chronic cerebral hypoperfusion alters the CypA-EMMPRIN-gelatinase pathway: Implications for vascular dementia.</name><description>Chronic cerebral hypoperfusion (CCH) is postulated to underlie multiple pathophysiological processes in vascular dementia (VaD), including extracellular matrix dysfunction. While several extracellular matrix proteins, namely cyclophilin A (CypA), extracellular matrix metalloproteinase inducer (EMMPRIN) and gelatinases (matrix metalloproteinases, MMP-2 and -9) have been investigated in acute stroke, their involvement in CCH and VaD remains unclear. In this study, CypA-EMMPRIN-gelatinase proteins were analysed in a clinical cohort of 36 aged, cognitively unimpaired subjects and 48 VaD patients, as well as in a bilateral carotid artery stenosis mouse model of CCH. Lower CypA and higher EMMPRIN levels were found in both VaD serum and CCH mouse brain. Furthermore, gelatinases were differentiall</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 May</publication><modification>2025-04-20T00:12:27.105Z</modification><creation>2025-04-20T00:12:27.105Z</creation></dates><accession>S-EPMC10108186</accession><cross_references><pubmed>36537035</pubmed><doi>10.1177/0271678X221146401</doi><doi>10.1177/0271678x221146401</doi></cross_references></HashMap>