000271971 001__ 271971
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000271971 1001_ $$0P:(DE-2719)9002951$$aDörner, Marc$$b0$$eFirst author$$udzne
000271971 245__ $$aNeuropsychiatric symptoms and lifelong mental activities in cerebral amyloid angiopathy - a cross-sectional study.
000271971 260__ $$aLondon$$bBioMed Central$$c2024
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000271971 520__ $$aWhile several studies in cerebral amyloid angiopathy (CAA) focus on cognitive function, data on neuropsychiatric symptoms (NPS) and lifelong mental activities in these patients are scarce. Since NPS are associated with functional impairment, faster cognitive decline and faster progression to death, replication studies in more diverse settings and samples are warranted.We prospectively recruited n = 69 CAA patients and n = 18 cognitively normal controls (NC). The number and severity of NPS were assessed using the Alzheimer's Disease (AD) Assessment Scale's (ADAS) noncognitive subscale. We applied different regression models exploring associations between NPS number or severity and group status (CAA vs. NC), CAA severity assessed with magnetic resonance imaging (MRI) or cognitive function (Mini-Mental State Examination (MMSE), ADAS cognitive subscale), adjusting for age, sex, years of education, arterial hypertension, AD pathology, and apolipoprotein E status. Mediation analyses were performed to test indirect effects of lifelong mental activities on CAA severity and NPS.Patients with CAA had 4.86 times (95% CI 2.20-10.73) more NPS and 3.56 units (95% CI 1.94-5.19) higher expected NPS severity than NC. Higher total CAA severity on MRI predicted 1.14 times (95% CI 1.01.-1.27) more NPS and 0.57 units (95% CI 0.19-0.95) higher expected NPS severity. More severe white matter hyperintensities were associated with 1.21 times more NPS (95% CI 1.05-1.39) and 0.63 units (95% CI 0.19-1.08) more severe NPS. NPS number (MMSE mean difference - 1.15, 95% CI -1.67 to -0.63; ADAS cognitive mean difference 1.91, 95% CI 1.26-2.56) and severity (MMSE - 0.55, 95% CI -0.80 to -0.30; ADAS cognitive mean difference 0.89, 95% CI 0.57-1.21) predicted lower cognitive function. Greater lifelong mental activities partially mediated the relationship between CAA severity and NPS (indirect effect 0.05, 95% CI 0.0007-0.13), and greater lifelong mental activities led to less pronounced CAA severity and thus to less NPS (indirect effect - 0.08, 95% CI -0.22 to -0.002).This study suggests that NPS are common in CAA, and that this relationship may be driven by CAA severity. Furthermore, NPS seem to be tied to lower cognitive function. However, lifelong mental activities might mitigate the impact of NPS in CAA.
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000271971 650_7 $$2Other$$aAlzheimer’s disease
000271971 650_7 $$2Other$$aCerebral amyloid angiopathy
000271971 650_7 $$2Other$$aDepression
000271971 650_7 $$2Other$$aLifelong mental activities
000271971 650_7 $$2Other$$aMagnetic resonance imaging
000271971 650_7 $$2Other$$aNeuropsychiatric symptoms
000271971 650_7 $$2Other$$aWhite matter hyperintensities
000271971 650_2 $$2MeSH$$aHumans
000271971 650_2 $$2MeSH$$aFemale
000271971 650_2 $$2MeSH$$aMale
000271971 650_2 $$2MeSH$$aAged
000271971 650_2 $$2MeSH$$aCross-Sectional Studies
000271971 650_2 $$2MeSH$$aCerebral Amyloid Angiopathy: diagnostic imaging
000271971 650_2 $$2MeSH$$aCerebral Amyloid Angiopathy: psychology
000271971 650_2 $$2MeSH$$aMagnetic Resonance Imaging
000271971 650_2 $$2MeSH$$aNeuropsychological Tests
000271971 650_2 $$2MeSH$$aMiddle Aged
000271971 650_2 $$2MeSH$$aCognitive Dysfunction: diagnostic imaging
000271971 650_2 $$2MeSH$$aCognitive Dysfunction: etiology
000271971 650_2 $$2MeSH$$aProspective Studies
000271971 650_2 $$2MeSH$$aSeverity of Illness Index
000271971 650_2 $$2MeSH$$aAged, 80 and over
000271971 7001_ $$aTyndall, Anthony$$b1
000271971 7001_ $$aHainc, Nicolin$$b2
000271971 7001_ $$avon Känel, Roland$$b3
000271971 7001_ $$0P:(DE-2719)2810407$$aNeumann, Katja$$b4$$udzne
000271971 7001_ $$aEuler, Sebastian$$b5
000271971 7001_ $$0P:(DE-2719)9000986$$aSchreiber, Frank$$b6$$udzne
000271971 7001_ $$0P:(DE-2719)9000797$$aUlbrich, Philipp$$b7$$udzne
000271971 7001_ $$aFuchs, Erelle$$b8
000271971 7001_ $$0P:(DE-2719)2813207$$aGarz, Cornelia$$b9$$udzne
000271971 7001_ $$0P:(DE-2719)2811614$$aGlanz, Wenzel$$b10$$udzne
000271971 7001_ $$0P:(DE-2719)9001011$$aButryn, Michaela$$b11$$udzne
000271971 7001_ $$aSchulze, Jan Ben$$b12
000271971 7001_ $$aSchiebler, Sarah Lavinia Florence$$b13
000271971 7001_ $$aJohn, Anna-Charlotte$$b14
000271971 7001_ $$aHildebrand, Annkatrin$$b15
000271971 7001_ $$0P:(DE-2719)9000921$$aHofmann, Andreas B$$b16
000271971 7001_ $$aMachetanz, Lena$$b17
000271971 7001_ $$aKirchebner, Johannes$$b18
000271971 7001_ $$0P:(DE-2719)9002214$$aTacik, Pawel$$b19$$udzne
000271971 7001_ $$aGrimm, Alexander$$b20
000271971 7001_ $$aJansen, Robin$$b21
000271971 7001_ $$0P:(DE-2719)9003204$$aPawlitzki, Marc$$b22$$udzne
000271971 7001_ $$0P:(DE-2719)2813348$$aHenneicke, Solveig$$b23$$udzne
000271971 7001_ $$0P:(DE-2719)9001989$$aBernal, Jose$$b24$$udzne
000271971 7001_ $$0P:(DE-2719)9000985$$aPerosa, Valentina$$b25$$udzne
000271971 7001_ $$0P:(DE-2719)2000005$$aDüzel, Emrah$$b26$$udzne
000271971 7001_ $$aMeuth, Sven G$$b27
000271971 7001_ $$0P:(DE-2719)2000035$$aVielhaber, Stefan$$b28$$udzne
000271971 7001_ $$0P:(DE-2719)9002178$$aMattern, Hendrik$$b29$$udzne
000271971 7001_ $$0P:(DE-2719)2812631$$aSchreiber, Stefanie$$b30$$eLast author$$udzne
000271971 773__ $$0PERI:(DE-600)2506521-X$$a10.1186/s13195-024-01519-3$$gVol. 16, no. 1, p. 196$$n1$$p196$$tAlzheimer's research & therapy$$v16$$x1758-9193$$y2024
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