<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Leitner D</submitter><funding>NIA NIH HHS</funding><funding>NIA</funding><pagination>9</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11263258</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>148(1)</volume><pubmed_abstract>Cerebral amyloid angiopathy (CAA) is characterized by amyloid beta (Aβ) deposition in cerebrovasculature. It is prevalent with aging and Alzheimer's disease (AD), associated with intracerebral hemorrhage, and contributes to cognitive deficits. To better understand molecular mechanisms, CAA(+) and CAA(-) vessels were microdissected from paraffin-embedded autopsy temporal cortex of age-matched Control (n = 10), mild cognitive impairment (MCI; n = 4), and sporadic AD (n = 6) cases, followed by label-free quantitative mass spectrometry. 257 proteins were differentially abundant in CAA(+) vessels compared to neighboring CAA(-) vessels in MCI, and 289 in AD (p &lt; 0.05, fold-change > 1.5). 84 proteins changed in the same direction in both groups, and many changed in the same direction among protei</pubmed_abstract><journal>Acta neuropathologica</journal><pubmed_title>Differences in the cerebral amyloid angiopathy proteome in Alzheimer's disease and mild cognitive impairment.</pubmed_title><pmcid>PMC11263258</pmcid><funding_grant_id>P30 AG072975</funding_grant_id><funding_grant_id>P30AG066512</funding_grant_id><funding_grant_id>P30 AG066512</funding_grant_id><funding_grant_id>P30 AG010161</funding_grant_id><funding_grant_id>P01AG060882</funding_grant_id><funding_grant_id>R01 AG017917</funding_grant_id><funding_grant_id>P01 AG060882</funding_grant_id><pubmed_authors>Suazo JI</pubmed_authors><pubmed_authors>Ueberheide B</pubmed_authors><pubmed_authors>Kanshin E</pubmed_authors><pubmed_authors>Thierry M</pubmed_authors><pubmed_authors>Pires G</pubmed_authors><pubmed_authors>Kavanagh T</pubmed_authors><pubmed_authors>Wisniewski T</pubmed_authors><pubmed_authors>Leitner D</pubmed_authors><pubmed_authors>Balcomb K</pubmed_authors><pubmed_authors>Schneider J</pubmed_authors><pubmed_authors>Drummond E</pubmed_authors></additional><is_claimable>false</is_claimable><name>Differences in the cerebral amyloid angiopathy proteome in Alzheimer's disease and mild cognitive impairment.</name><description>Cerebral amyloid angiopathy (CAA) is characterized by amyloid beta (Aβ) deposition in cerebrovasculature. It is prevalent with aging and Alzheimer's disease (AD), associated with intracerebral hemorrhage, and contributes to cognitive deficits. To better understand molecular mechanisms, CAA(+) and CAA(-) vessels were microdissected from paraffin-embedded autopsy temporal cortex of age-matched Control (n = 10), mild cognitive impairment (MCI; n = 4), and sporadic AD (n = 6) cases, followed by label-free quantitative mass spectrometry. 257 proteins were differentially abundant in CAA(+) vessels compared to neighboring CAA(-) vessels in MCI, and 289 in AD (p &lt; 0.05, fold-change > 1.5). 84 proteins changed in the same direction in both groups, and many changed in the same direction among protei</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Jul</publication><modification>2026-06-01T20:29:44.894Z</modification><creation>2025-05-18T13:26:45.89Z</creation></dates><accession>S-EPMC11263258</accession><cross_references><pubmed>39039355</pubmed><doi>10.1007/s00401-024-02767-1</doi></cross_references></HashMap>