FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2767102024> ?p ?o ?g. }

• W2767102024 abstract "Vascular risk factors have been increasingly implicated in Alzheimer's disease (AD). Blood pressure and decreased cerebral blood flow (CBF) are of particular interest given their links to AD biomarkers and clinical progression. We therefore hypothesized that elevated ratio of blood pressure to CBF, indicative of cerebrovascular resistance, would predict amyloid retention, cognitive decline, cortical thinning, and progression to dementia over a 2-year period, independent of neuronal metabolism. Older adults with (n = 33) and without (n = 199) AD underwent arterial spin labeling magnetic resonance imaging to measure regional CBF in brain regions susceptible to aging and AD. An estimated cerebrovascular resistance index (CVRi) was then calculated as the ratio of mean arterial pressure to regional CBF. Positron emission tomography with florbetapir-fluorine-18 (18F) and fludeoxyglucose was used to quantify amyloid retention and neuronal metabolism, respectively. Non-demented participants were classified as Aβ– or Aβ+ based on florbetapir-indexed amyloid load. Cognitive performance was evaluated via annual assessments of global cognition, memory, and executive function. Linear mixed models and regression were used to assess CVRi prediction of cognitive performance, amyloid, and atrophy over 2 years. CVRi prediction of progression to dementia was evaluated using logistic regression. CVRi was significantly elevated in non-demented Aβ+ versus Aβ– participants, with further elevation observed in AD patients. CVRi group differences were also of greater statistical effect size and encompassed a greater number of brain regions, than those for CBF alone, including frontal, parietal, temporal, and hippocampal areas. Cognitive decline over 2-year follow-up was accelerated by elevated baseline CVRi, particularly for amyloid-positive individuals. Higher CVRi was also associated with elevated inferior temporal amyloid retention and cortical thinning 2 years later. Finally, increased CVRi predicted greater progression to dementia, beyond that attributable to amyloid-positivity. Findings suggest that increased cerebrovascular resistance may represent a previously unrecognized contributor to Alzheimer's disease that is independent of neuronal hypometabolism, predates changes in brain perfusion, exacerbates and works synergistically with amyloidosis to produce cognitive decline, and drives amyloid-independent brain atrophy during the earliest stage of disease." @default.
• W2767102024 created "2017-11-10" @default.
• W2767102024 creator A5020498061 @default.
• W2767102024 creator A5042725452 @default.
• W2767102024 date "2017-07-01" @default.
• W2767102024 modified "2023-10-16" @default.
• W2767102024 title "[P3-366]: CEREBROVASCULAR RESISTANCE AND CEREBRAL AMYLOIDOSIS: EFFECTS ON COGNITIVE DECLINE, CORTICAL ATROPHY AND PROGRESSION TO DEMENTIA" @default.
• W2767102024 doi "https://doi.org/10.1016/j.jalz.2017.06.1582" @default.
• W2767102024 hasPublicationYear "2017" @default.
• W2767102024 type Work @default.
• W2767102024 sameAs 2767102024 @default.
• W2767102024 citedByCount "0" @default.
• W2767102024 crossrefType "journal-article" @default.
• W2767102024 hasAuthorship W2767102024A5020498061 @default.
• W2767102024 hasAuthorship W2767102024A5042725452 @default.
• W2767102024 hasBestOaLocation W27671020241 @default.
• W2767102024 hasConcept C126322002 @default.
• W2767102024 hasConcept C126838900 @default.
• W2767102024 hasConcept C143409427 @default.
• W2767102024 hasConcept C15744967 @default.
• W2767102024 hasConcept C157767197 @default.
• W2767102024 hasConcept C164705383 @default.
• W2767102024 hasConcept C169760540 @default.
• W2767102024 hasConcept C2775842073 @default.
• W2767102024 hasConcept C2779134260 @default.
• W2767102024 hasConcept C2779483572 @default.
• W2767102024 hasConcept C2781172350 @default.
• W2767102024 hasConcept C2984863031 @default.
• W2767102024 hasConcept C67739388 @default.
• W2767102024 hasConcept C71924100 @default.
• W2767102024 hasConceptScore W2767102024C126322002 @default.
• W2767102024 hasConceptScore W2767102024C126838900 @default.
• W2767102024 hasConceptScore W2767102024C143409427 @default.
• W2767102024 hasConceptScore W2767102024C15744967 @default.
• W2767102024 hasConceptScore W2767102024C157767197 @default.
• W2767102024 hasConceptScore W2767102024C164705383 @default.
• W2767102024 hasConceptScore W2767102024C169760540 @default.
• W2767102024 hasConceptScore W2767102024C2775842073 @default.
• W2767102024 hasConceptScore W2767102024C2779134260 @default.
• W2767102024 hasConceptScore W2767102024C2779483572 @default.
• W2767102024 hasConceptScore W2767102024C2781172350 @default.
• W2767102024 hasConceptScore W2767102024C2984863031 @default.
• W2767102024 hasConceptScore W2767102024C67739388 @default.
• W2767102024 hasConceptScore W2767102024C71924100 @default.
• W2767102024 hasIssue "7S_Part_22" @default.
• W2767102024 hasLocation W27671020241 @default.
• W2767102024 hasOpenAccess W2767102024 @default.
• W2767102024 hasPrimaryLocation W27671020241 @default.
• W2767102024 hasRelatedWork W1885211110 @default.
• W2767102024 hasRelatedWork W1968355414 @default.
• W2767102024 hasRelatedWork W2165309011 @default.
• W2767102024 hasRelatedWork W2172455872 @default.
• W2767102024 hasRelatedWork W2406467936 @default.
• W2767102024 hasRelatedWork W2517969440 @default.
• W2767102024 hasRelatedWork W2797010042 @default.
• W2767102024 hasRelatedWork W2895553013 @default.
• W2767102024 hasRelatedWork W2899001075 @default.
• W2767102024 hasRelatedWork W4376106102 @default.
• W2767102024 hasVolume "13" @default.
• W2767102024 isParatext "false" @default.
• W2767102024 isRetracted "false" @default.
• W2767102024 magId "2767102024" @default.
• W2767102024 workType "article" @default.