Matches in SemOpenAlex for { <https://semopenalex.org/work/W2897051975> ?p ?o ?g. }
Showing items 1 to 76 of
76
with 100 items per page.
- W2897051975 abstract "Alzheimer's disease (AD) is characterized by amyloid-β (Aβ) accumulation and spreading of tau, which is thought to cause neurodegeneration predominantly in the medial temporal lobe that can be visualized as atrophy. We wanted to examine if other pathologic processes, specifically white matter lesions (WML), were associated with atrophy of these regions. Cerebrospinal fluid (CSF) levels of Aβ40, Aβ42, and phosphorylated tau (p-tau), and magnetic resonance imaging (MRI) measures of WML load and thickness and volume of regional brain structures were studied cross-sectionally in participants in The Swedish BioFINDER Study including subjects with mild cognitive impairment (MCI) and subjective cognitive decline (SCD), as well as cognitively normal (CN) controls. Amyloid pathology was defined as an abnormal CSF Aβ42/Aβ40 ratio and tau pathology as levels of p-tau. FreeSurfer software was used for automated segmentation of brain structures. Multiple linear regressions were performed to estimate the associations between CSF/MRI measures and hippocampal volume/regional cortical thickness, adjusting for age, sex, and diagnosis (CN, SCD, MCI), as well as total intracranial volume in models including hippocampal volume (HV). Univariate as well as multivariate analyses were performed for the different CSF/MRI measures. Aβ pathology was associated with HV and temporal, frontal and parietal cortical thickness. Tau pathology was associated with parietal cortical thickness. Total WML load was associated with HV and temporal and frontal cortical thickness. There was no association between any of the CSF/MRI measures and occipital cortical thickness. Multivariate analysis showed independent and similar effects of CSF Aβ42/40 and WML on HV and temporal cortical thickness. Aβ pathology and white-matter lesions are both independently associated with hippocampal volume and temporal cortical thickness, which shows that atrophy in these regions are not specific to AD." @default.
- W2897051975 created "2018-10-26" @default.
- W2897051975 creator A5023889784 @default.
- W2897051975 creator A5024645775 @default.
- W2897051975 creator A5066503440 @default.
- W2897051975 creator A5066655847 @default.
- W2897051975 date "2018-07-01" @default.
- W2897051975 modified "2023-10-16" @default.
- W2897051975 title "P1‐373: βETA‐AMYLOID AND WHITE MATTER LESIONS ARE INDEPENDENTLY ASSOCIATED WITH HIPPOCAMPAL ATROPHY AND REDUCED CORTICAL TEMPORAL THICKNESS" @default.
- W2897051975 doi "https://doi.org/10.1016/j.jalz.2018.06.381" @default.
- W2897051975 hasPublicationYear "2018" @default.
- W2897051975 type Work @default.
- W2897051975 sameAs 2897051975 @default.
- W2897051975 citedByCount "0" @default.
- W2897051975 crossrefType "journal-article" @default.
- W2897051975 hasAuthorship W2897051975A5023889784 @default.
- W2897051975 hasAuthorship W2897051975A5024645775 @default.
- W2897051975 hasAuthorship W2897051975A5066503440 @default.
- W2897051975 hasAuthorship W2897051975A5066655847 @default.
- W2897051975 hasConcept C126838900 @default.
- W2897051975 hasConcept C142724271 @default.
- W2897051975 hasConcept C143409427 @default.
- W2897051975 hasConcept C146638467 @default.
- W2897051975 hasConcept C148762608 @default.
- W2897051975 hasConcept C15744967 @default.
- W2897051975 hasConcept C169760540 @default.
- W2897051975 hasConcept C2777633098 @default.
- W2897051975 hasConcept C2778186239 @default.
- W2897051975 hasConcept C2779134260 @default.
- W2897051975 hasConcept C2779651940 @default.
- W2897051975 hasConcept C2781073650 @default.
- W2897051975 hasConcept C2781099131 @default.
- W2897051975 hasConcept C2781172350 @default.
- W2897051975 hasConcept C2781192897 @default.
- W2897051975 hasConcept C502032728 @default.
- W2897051975 hasConcept C58693492 @default.
- W2897051975 hasConcept C65835030 @default.
- W2897051975 hasConcept C71924100 @default.
- W2897051975 hasConceptScore W2897051975C126838900 @default.
- W2897051975 hasConceptScore W2897051975C142724271 @default.
- W2897051975 hasConceptScore W2897051975C143409427 @default.
- W2897051975 hasConceptScore W2897051975C146638467 @default.
- W2897051975 hasConceptScore W2897051975C148762608 @default.
- W2897051975 hasConceptScore W2897051975C15744967 @default.
- W2897051975 hasConceptScore W2897051975C169760540 @default.
- W2897051975 hasConceptScore W2897051975C2777633098 @default.
- W2897051975 hasConceptScore W2897051975C2778186239 @default.
- W2897051975 hasConceptScore W2897051975C2779134260 @default.
- W2897051975 hasConceptScore W2897051975C2779651940 @default.
- W2897051975 hasConceptScore W2897051975C2781073650 @default.
- W2897051975 hasConceptScore W2897051975C2781099131 @default.
- W2897051975 hasConceptScore W2897051975C2781172350 @default.
- W2897051975 hasConceptScore W2897051975C2781192897 @default.
- W2897051975 hasConceptScore W2897051975C502032728 @default.
- W2897051975 hasConceptScore W2897051975C58693492 @default.
- W2897051975 hasConceptScore W2897051975C65835030 @default.
- W2897051975 hasConceptScore W2897051975C71924100 @default.
- W2897051975 hasIssue "7S_Part_8" @default.
- W2897051975 hasLocation W28970519751 @default.
- W2897051975 hasOpenAccess W2897051975 @default.
- W2897051975 hasPrimaryLocation W28970519751 @default.
- W2897051975 hasRelatedWork W2020961462 @default.
- W2897051975 hasRelatedWork W2045661260 @default.
- W2897051975 hasRelatedWork W2085696301 @default.
- W2897051975 hasRelatedWork W2088129757 @default.
- W2897051975 hasRelatedWork W2161684081 @default.
- W2897051975 hasRelatedWork W2163980871 @default.
- W2897051975 hasRelatedWork W2399531985 @default.
- W2897051975 hasRelatedWork W2897573092 @default.
- W2897051975 hasRelatedWork W3115446597 @default.
- W2897051975 hasRelatedWork W4205371055 @default.
- W2897051975 hasVolume "14" @default.
- W2897051975 isParatext "false" @default.
- W2897051975 isRetracted "false" @default.
- W2897051975 magId "2897051975" @default.
- W2897051975 workType "article" @default.