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A longitudinal investigation of Aβ, anxiety, depression, and mild cognitive impairment
A. Pink, J. Krell-Roesch, JA. Syrjanen, M. Vassilaki, VJ. Lowe, P. Vemuri, GB. Stokin, TJ. Christianson, WK. Kremers, CR. Jack, DS. Knopman, RC. Petersen, YE. Geda
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články
Grantová podpora
R01 AG057708
NIA NIH HHS - United States
PubMed
34877794
DOI
10.1002/alz.12504
Knihovny.cz E-zdroje
- MeSH
- Alzheimerova nemoc * psychologie MeSH
- amyloidní beta-protein metabolismus MeSH
- aniliny MeSH
- deprese epidemiologie psychologie MeSH
- kognitivní dysfunkce * diagnostické zobrazování epidemiologie psychologie MeSH
- lidé MeSH
- mozek metabolismus MeSH
- neuropsychologické testy MeSH
- pozitronová emisní tomografie metody MeSH
- úzkost epidemiologie psychologie MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
INTRODUCTION: We investigated the longitudinal relationship between cortical amyloid deposition, anxiety, and depression and the risk of incident mild cognitive impairment (MCI). METHODS: We followed 1440 community-dwelling, cognitively unimpaired individuals aged ≥ 50 years for a median of 5.5 years. Clinical anxiety and depression were assessed using Beck Anxiety and Depression Inventories (BAI, BDI-II). Cortical amyloid beta (Aβ) was measured by Pittsburgh compound B positron emission tomography (PiB-PET) and elevated deposition (PiB+) was defined as standardized uptake value ratio ≥ 1.48. We calculated Cox proportional hazards models with age as the time scale, adjusted for sex, education, and medical comorbidity. RESULTS: Cortical Aβ deposition (PiB+) independent of anxiety (BAI ≥ 10) or depression (BDI-II ≥ 13) increased the risk of MCI. There was a significant additive interaction between PiB+ and anxiety (joint effect hazard ratio 6.77; 95% confidence interval 3.58-12.79; P = .031) that is, being PiB+ and having anxiety further amplified the risk of MCI. DISCUSSION: Anxiety modified the association between PiB+ and incident MCI.
Department of Geriatrics Paracelsus Medical University Salzburg Austria
Department of Neurology Barrow Neurological Institute Phoenix Arizona USA
Department of Neurology Mayo Clinic Rochester Minnesota USA
Department of Quantitative Health Sciences Mayo Clinic Rochester Rochester Minnesota USA
Department of Radiology Mayo Clinic Rochester Minnesota USA
Institute of Sports and Sports Science Karlsruhe Institute of Technology Karlsruhe Germany
International Clinical Research Center St Anne Hospital Brno Czech Republic
Citace poskytuje Crossref.org
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- $a INTRODUCTION: We investigated the longitudinal relationship between cortical amyloid deposition, anxiety, and depression and the risk of incident mild cognitive impairment (MCI). METHODS: We followed 1440 community-dwelling, cognitively unimpaired individuals aged ≥ 50 years for a median of 5.5 years. Clinical anxiety and depression were assessed using Beck Anxiety and Depression Inventories (BAI, BDI-II). Cortical amyloid beta (Aβ) was measured by Pittsburgh compound B positron emission tomography (PiB-PET) and elevated deposition (PiB+) was defined as standardized uptake value ratio ≥ 1.48. We calculated Cox proportional hazards models with age as the time scale, adjusted for sex, education, and medical comorbidity. RESULTS: Cortical Aβ deposition (PiB+) independent of anxiety (BAI ≥ 10) or depression (BDI-II ≥ 13) increased the risk of MCI. There was a significant additive interaction between PiB+ and anxiety (joint effect hazard ratio 6.77; 95% confidence interval 3.58-12.79; P = .031) that is, being PiB+ and having anxiety further amplified the risk of MCI. DISCUSSION: Anxiety modified the association between PiB+ and incident MCI.
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