Evidence map›Paper›PMID 39232823›Full record

ArticleAlzheimer's research & therapy2024

Neuropsychiatric symptoms and lifelong mental activities in cerebral amyloid angiopathy - a cross-sectional study.

Marc Dörner, Anthony Tyndall, Nicolin Hainc, Roland von Känel, Katja Neumann, Sebastian Euler, Frank Schreiber, Philipp Arndt, Erelle Fuchs, Cornelia Garz and 21 more

Abstract read
In one paragraph

Article in Alzheimer's research & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

  1. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

31 authors.

Marc DörnerGerman Center for Neurodegenerative Diseases (DZNE) within the Helmholtz Association, 39120, Magdeburg, Germany. marc.doerner@usz.ch.
Anthony TyndallDepartment of Neuroradiology, Clinical Neuroscience Center, University Hospital Zurich, University of Zurich, Zurich, 8091, Switzerland.
Nicolin HaincDepartment of Neuroradiology, Clinical Neuroscience Center, University Hospital Zurich, University of Zurich, Zurich, 8091, Switzerland.
Roland von KänelDepartment of Consultation-Liaison-Psychiatry and Psychosomatic Medicine, University Hospital Zurich, University of Zurich, Culmannstrasse 8, Zurich, 8091, Switzerland.
Katja NeumannDepartment of Neurology, Otto-von-Guericke University, 39120, Magdeburg, Germany.
Sebastian EulerDepartment of Consultation-Liaison-Psychiatry and Psychosomatic Medicine, University Hospital Zurich, University of Zurich, Culmannstrasse 8, Zurich, 8091, Switzerland.
Frank SchreiberGerman Center for Neurodegenerative Diseases (DZNE) within the Helmholtz Association, 39120, Magdeburg, Germany.
Philipp ArndtGerman Center for Neurodegenerative Diseases (DZNE) within the Helmholtz Association, 39120, Magdeburg, Germany.
Erelle FuchsDepartment of Neuroradiology, Otto-von-Guericke University, 39120, Magdeburg, Germany.
Cornelia GarzGerman Center for Neurodegenerative Diseases (DZNE) within the Helmholtz Association, 39120, Magdeburg, Germany.
Wenzel GlanzGerman Center for Neurodegenerative Diseases (DZNE) within the Helmholtz Association, 39120, Magdeburg, Germany.
Michaela ButrynGerman Center for Neurodegenerative Diseases (DZNE) within the Helmholtz Association, 39120, Magdeburg, Germany.
Jan Ben SchulzeDepartment of Consultation-Liaison-Psychiatry and Psychosomatic Medicine, University Hospital Zurich, University of Zurich, Culmannstrasse 8, Zurich, 8091, Switzerland.
Sarah Lavinia Florence SchieblerDepartment of Consultation-Liaison-Psychiatry and Psychosomatic Medicine, University Hospital Zurich, University of Zurich, Culmannstrasse 8, Zurich, 8091, Switzerland.
Anna-Charlotte JohnDepartment of Neurology, Otto-von-Guericke University, 39120, Magdeburg, Germany.
Annkatrin HildebrandDepartment of Neurology, Otto-von-Guericke University, 39120, Magdeburg, Germany.
Andreas B HofmannDepartment of Psychiatry, Psychotherapy, and Psychosomatics, University Hospital of Psychiatry Zurich, University of Zurich, Zurich, 8032, Switzerland.
Lena MachetanzDepartment of Forensic Psychiatry, University Hospital of Psychiatry Zurich, University of Zurich, Zurich, 8032, Switzerland.
Johannes KirchebnerDepartment of Forensic Psychiatry, University Hospital of Psychiatry Zurich, University of Zurich, Zurich, 8032, Switzerland.
Pawel TacikDepartment of Parkinson's Disease, Sleep and Movement Disorders, University Hospital Bonn, 53127, Bonn, Germany.
Alexander GrimmCenter for Neurology, Tuebingen University Hospital and Hertie-Institute for Clinical Brain Research, Eberhard Karls University, 72076, Tuebingen, Tuebingen, Germany.
Robin JansenDepartment of Neurology, Heinrich Heine University, 40225, Düsseldorf, Germany.
Marc PawlitzkiDepartment of Neurology, Heinrich Heine University, 40225, Düsseldorf, Germany.
Solveig HenneickeGerman Center for Neurodegenerative Diseases (DZNE) within the Helmholtz Association, 39120, Magdeburg, Germany.
Jose BernalGerman Center for Neurodegenerative Diseases (DZNE) within the Helmholtz Association, 39120, Magdeburg, Germany.
Valentina PerosaJ. Philip Kistler Stroke Research Center, Massachusetts General Hospital, Boston, MA, 02114, USA.
Emrah DüzelGerman Center for Neurodegenerative Diseases (DZNE) within the Helmholtz Association, 39120, Magdeburg, Germany.
Sven G MeuthDepartment of Neurology, Heinrich Heine University, 40225, Düsseldorf, Germany.
Stefan VielhaberDepartment of Neurology, Otto-von-Guericke University, 39120, Magdeburg, Germany.
Hendrik MatternGerman Center for Neurodegenerative Diseases (DZNE) within the Helmholtz Association, 39120, Magdeburg, Germany.
Stefanie SchreiberGerman Center for Neurodegenerative Diseases (DZNE) within the Helmholtz Association, 39120, Magdeburg, Germany. stefanie.schreiber@med.ovgu.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWhile 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.

methodsWe 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.

resultsPatients 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). DISCUSSION: 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.

Indexed as

Cerebral Amyloid AngiopathyMagnetic Resonance ImagingNeuropsychological TestsAgedAged, 80 and overCognitive DysfunctionCross-Sectional StudiesFemaleHumansMaleMiddle AgedProspective StudiesSeverity of Illness IndexAlzheimer’s diseaseCerebral amyloid angiopathyDepressionLifelong mental activitiesMagnetic resonance imagingNeuropsychiatric symptomsWhite matter hyperintensities

Identifiers

PMID39232823
PMCPMC11375846

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.