<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Kiss T</submitter><funding>NIA NIH HHS</funding><funding>NINDS NIH HHS</funding><funding>NIGMS NIH HHS</funding><funding>National Institute on Aging</funding><pagination>619-630</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6885080</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>41(5)</volume><pubmed_abstract>Age-related impairment of angiogenesis likely has a critical role in cerebromicrovascular rarefaction and development of vascular cognitive impairment and dementia (VCID) in the elderly. Recently, we demonstrated that aging is associated with NAD&lt;sup>+&lt;/sup> depletion in the vasculature and that administration of NAD&lt;sup>+&lt;/sup> precursors exerts potent anti-aging vascular effects, rescuing endothelium-mediated vasodilation in the cerebral circulation and improving cerebral blood supply. The present study was designed to elucidate how treatment with nicotinamide mononucleotide (NMN), a key NAD&lt;sup>+&lt;/sup> intermediate, impacts age-related impairment of endothelial angiogenic processes. Using cerebromicrovascular endothelial cells (CMVECs) isolated from young and aged F344xBN rats, we demon</pubmed_abstract><journal>GeroScience</journal><pubmed_title>Nicotinamide mononucleotide (NMN) treatment attenuates oxidative stress and rescues angiogenic capacity in aged cerebromicrovascular endothelial cells: a potential mechanism for the prevention of vascular cognitive impairment.</pubmed_title><pmcid>PMC6885080</pmcid><funding_grant_id>U54 GM104938</funding_grant_id><funding_grant_id>R01 AG047879</funding_grant_id><funding_grant_id>R01-AG038747</funding_grant_id><funding_grant_id>R01-AG047879</funding_grant_id><funding_grant_id>P20 GM125528</funding_grant_id><funding_grant_id>P20 GM103447</funding_grant_id><funding_grant_id>R01 NS056218</funding_grant_id><funding_grant_id>R01 AG055395</funding_grant_id><funding_grant_id>R01 NS100782</funding_grant_id><funding_grant_id>R01-AG055395</funding_grant_id><pubmed_authors>Valcarcel-Ares MN</pubmed_authors><pubmed_authors>Farkas E</pubmed_authors><pubmed_authors>Zhang XA</pubmed_authors><pubmed_authors>Yabluchanskiy A</pubmed_authors><pubmed_authors>Kiss T</pubmed_authors><pubmed_authors>Balasubramanian P</pubmed_authors><pubmed_authors>Lipecz A</pubmed_authors><pubmed_authors>Ungvari Z</pubmed_authors><pubmed_authors>Bari F</pubmed_authors><pubmed_authors>Tarantini S</pubmed_authors><pubmed_authors>Csiszar A</pubmed_authors><pubmed_authors>Csipo T</pubmed_authors><pubmed_authors>Reglodi D</pubmed_authors></additional><is_claimable>false</is_claimable><name>Nicotinamide mononucleotide (NMN) treatment attenuates oxidative stress and rescues angiogenic capacity in aged cerebromicrovascular endothelial cells: a potential mechanism for the prevention of vascular cognitive impairment.</name><description>Age-related impairment of angiogenesis likely has a critical role in cerebromicrovascular rarefaction and development of vascular cognitive impairment and dementia (VCID) in the elderly. Recently, we demonstrated that aging is associated with NAD&lt;sup>+&lt;/sup> depletion in the vasculature and that administration of NAD&lt;sup>+&lt;/sup> precursors exerts potent anti-aging vascular effects, rescuing endothelium-mediated vasodilation in the cerebral circulation and improving cerebral blood supply. The present study was designed to elucidate how treatment with nicotinamide mononucleotide (NMN), a key NAD&lt;sup>+&lt;/sup> intermediate, impacts age-related impairment of endothelial angiogenic processes. Using cerebromicrovascular endothelial cells (CMVECs) isolated from young and aged F344xBN rats, we demon</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Oct</publication><modification>2025-04-26T10:11:02.382Z</modification><creation>2020-05-21T23:25:48Z</creation></dates><accession>S-EPMC6885080</accession><cross_references><pubmed>31144244</pubmed><doi>10.1007/s11357-019-00074-2</doi></cross_references></HashMap>