Detail
Article
Online article
FT
Medvik - BMC
  • Something wrong with this record ?

Interactions Between Neuropsychiatric Symptoms and Alzheimer's Disease Neuroimaging Biomarkers in Predicting Longitudinal Cognitive Decline

A. Pink, J. Krell-Roesch, JA. Syrjanen, LR. Christenson, VJ. Lowe, P. Vemuri, JA. Fields, GB. Stokin, WK. Kremers, EL. Scharf, CR. Jack, DS. Knopman, RC. Petersen, M. Vassilaki, YE. Geda

. 2023 ; 5 (1) : 4-15. [pub] 20230120

Status not-indexed Language English Country United States

Document type Journal Article

Persistent link   https://www.medvik.cz/link/bmc23002614

Grant support
R33 AG058738 NIA NIH HHS - United States

OBJECTIVE: To examine interactions between Neuropsychiatric symptoms (NPS) with Pittsburgh Compound B (PiB) and fluorodeoxyglucose positron emission tomography (FDG-PET) in predicting cognitive trajectories. METHODS: We conducted a longitudinal study in the setting of the population-based Mayo Clinic Study of Aging in Olmsted County, MN, involving 1581 cognitively unimpaired (CU) persons aged ≥50 years (median age 71.83 years, 54.0% males, 27.5% APOE ɛ4 carriers). NPS at baseline were assessed using the Neuropsychiatric Inventory Questionnaire (NPI-Q). Brain glucose hypometabolism was defined as a SUVR ≤ 1.47 (measured by FDG-PET) in regions typically affected in Alzheimer's disease. Abnormal cortical amyloid deposition was measured using PiB-PET (SUVR ≥ 1.48). Neuropsychological testing was done approximately every 15 months, and we calculated global and domain-specific (memory, language, attention, and visuospatial skills) cognitive z-scores. We ran linear mixed-effect models to examine the associations and interactions between NPS at baseline and z-scored PiB- and FDG-PET SUVRs in predicting cognitive z-scores adjusted for age, sex, education, and previous cognitive testing. RESULTS: Individuals at the average PiB and without NPS at baseline declined over time on cognitive z-scores. Those with increased PiB at baseline declined faster (two-way interaction), and those with increased PiB and NPS declined even faster (three-way interaction). We observed interactions between time, increased PiB and anxiety or irritability indicating accelerated decline on global z-scores, and between time, increased PiB and several NPS (e.g., agitation) showing faster domain-specific decline, especially on the attention domain. CONCLUSIONS: NPS and increased brain amyloid deposition synergistically interact in accelerating global and domain-specific cognitive decline among CU persons at baseline.

References provided by Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc23002614
003      
CZ-PrNML
005      
20230421100158.0
007      
ta
008      
230413s2023 xxu f 000 0|eng||
009      
AR
024    7_
$a 10.1176/appi.prcp.20220036 $2 doi
035    __
$a (PubMed)36909142
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a xxu
100    1_
$a Pink, Anna $u First Department of Medicine Paracelsus Medical University Salzburg Austria
245    10
$a Interactions Between Neuropsychiatric Symptoms and Alzheimer's Disease Neuroimaging Biomarkers in Predicting Longitudinal Cognitive Decline / $c A. Pink, J. Krell-Roesch, JA. Syrjanen, LR. Christenson, VJ. Lowe, P. Vemuri, JA. Fields, GB. Stokin, WK. Kremers, EL. Scharf, CR. Jack, DS. Knopman, RC. Petersen, M. Vassilaki, YE. Geda
520    9_
$a OBJECTIVE: To examine interactions between Neuropsychiatric symptoms (NPS) with Pittsburgh Compound B (PiB) and fluorodeoxyglucose positron emission tomography (FDG-PET) in predicting cognitive trajectories. METHODS: We conducted a longitudinal study in the setting of the population-based Mayo Clinic Study of Aging in Olmsted County, MN, involving 1581 cognitively unimpaired (CU) persons aged ≥50 years (median age 71.83 years, 54.0% males, 27.5% APOE ɛ4 carriers). NPS at baseline were assessed using the Neuropsychiatric Inventory Questionnaire (NPI-Q). Brain glucose hypometabolism was defined as a SUVR ≤ 1.47 (measured by FDG-PET) in regions typically affected in Alzheimer's disease. Abnormal cortical amyloid deposition was measured using PiB-PET (SUVR ≥ 1.48). Neuropsychological testing was done approximately every 15 months, and we calculated global and domain-specific (memory, language, attention, and visuospatial skills) cognitive z-scores. We ran linear mixed-effect models to examine the associations and interactions between NPS at baseline and z-scored PiB- and FDG-PET SUVRs in predicting cognitive z-scores adjusted for age, sex, education, and previous cognitive testing. RESULTS: Individuals at the average PiB and without NPS at baseline declined over time on cognitive z-scores. Those with increased PiB at baseline declined faster (two-way interaction), and those with increased PiB and NPS declined even faster (three-way interaction). We observed interactions between time, increased PiB and anxiety or irritability indicating accelerated decline on global z-scores, and between time, increased PiB and several NPS (e.g., agitation) showing faster domain-specific decline, especially on the attention domain. CONCLUSIONS: NPS and increased brain amyloid deposition synergistically interact in accelerating global and domain-specific cognitive decline among CU persons at baseline.
590    __
$a NEINDEXOVÁNO
655    _2
$a časopisecké články $7 D016428
700    1_
$a Krell-Roesch, Janina $u Department of Quantitative Health Sciences Mayo Clinic Rochester Rochester Minnesota USA $u Institute of Sports and Sports Science Karlsruhe Institute of Technology Karlsruhe Germany
700    1_
$a Syrjanen, Jeremy A $u Department of Quantitative Health Sciences Mayo Clinic Rochester Rochester Minnesota USA
700    1_
$a Christenson, Luke R $u Department of Quantitative Health Sciences Mayo Clinic Rochester Rochester Minnesota USA
700    1_
$a Lowe, Val J $u Department of Radiology Mayo Clinic Rochester Rochester Minnesota USA
700    1_
$a Vemuri, Prashanthi $u Department of Radiology Mayo Clinic Rochester Rochester Minnesota USA
700    1_
$a Fields, Julie A $u Department of Psychiatry and Psychology Mayo Clinic Rochester Rochester Minnesota USA
700    1_
$a Stokin, Gorazd B $u International Clinical Research Center/St. Anne Hospital Brno Czech Republic
700    1_
$a Kremers, Walter K $u Department of Quantitative Health Sciences Mayo Clinic Rochester Rochester Minnesota USA
700    1_
$a Scharf, Eugene L $u Department of Neurology Mayo Clinic Rochester Rochester Minnesota USA
700    1_
$a Jack, Clifford R $u Department of Radiology Mayo Clinic Rochester Rochester Minnesota USA
700    1_
$a Knopman, David S $u Department of Neurology Mayo Clinic Rochester Rochester Minnesota USA
700    1_
$a Petersen, Ronald C $u Department of Quantitative Health Sciences Mayo Clinic Rochester Rochester Minnesota USA $u Department of Neurology Mayo Clinic Rochester Rochester Minnesota USA
700    1_
$a Vassilaki, Maria $u Department of Quantitative Health Sciences Mayo Clinic Rochester Rochester Minnesota USA
700    1_
$a Geda, Yonas E $u Department of Neurology Franke Global Neuroscience Education Center Barrow Neurological Institute Phoenix Arizona USA
773    0_
$w MED00210753 $t Psychiatric research and clinical practice $x 2575-5609 $g Roč. 5, č. 1 (2023), s. 4-15
856    41
$u https://pubmed.ncbi.nlm.nih.gov/36909142 $y Pubmed
910    __
$a ABA008 $b sig $c sign $y p $z 0
990    __
$a 20230413 $b ABA008
991    __
$a 20230421100150 $b ABA008
999    __
$a ok $b bmc $g 1922613 $s 1188821
BAS    __
$a 3
BAS    __
$a PreBMC-PubMed-not-MEDLINE
BMC    __
$a 2023 $b 5 $c 1 $d 4-15 $e 20230120 $i 2575-5609 $m Psychiatric research and clinical practice $n Psychiatr Res Clin Pract $x MED00210753
GRA    __
$a R33 AG058738 $p NIA NIH HHS $2 United States
LZP    __
$a Pubmed-20230413

Find record

Citation metrics

Archiving options