Evidence map›Paper›PMID 33484978›Full record

ArticleParkinsonism & related disorders2021

Cognitive impairment in Parkinson's disease is associated with Default Mode Network subsystem connectivity and cerebrospinal fluid Aβ.

Pardis Zarifkar, Jeehyun Kim, Christian La, Kai Zhang, Sophie YorkWilliams, Taylor F Levine, Lu Tian, Per Borghammer, Kathleen L Poston

Abstract read
In one paragraph

Article in Parkinsonism & related disorders, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
–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

20 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  14. Morphological basis of Parkinson disease-associated cognitive impairment: an update.Journal of neural transmission (Vienna, Austria : 1996) · 2022
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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

9 authors.

Pardis ZarifkarDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305, USA; Department of Nuclear Medicine and PET, Aarhus University Hospital, Denmark. Electronic address: pardis.zarifkar@regionh.dk.
Jeehyun KimDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305, USA. Electronic address: jehn92@gmail.com.
Christian LaDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305, USA. Electronic address: christian.la013@gmail.com.
Kai ZhangDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305, USA. Electronic address: kyezhang@gmail.com.
Sophie YorkWilliamsDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305, USA; Department of Psychology and Neuroscience, University of Colorado, Boulder, CO, 80309, USA. Electronic address: sophie.yorkwilliams@gmail.com.
Taylor F LevineDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305, USA; Department of Psychological & Brain Sciences, Washington University, 1 Brookings Drive, St. Louis, MO, 63130, USA. Electronic address: trhendershott@wustl.edu.
Lu TianDepartment of Biomedical Data Science, Stanford University School of Medicine, 150 Governor's Lane, Stanford, CA, 94305, USA. Electronic address: lutian@stanford.edu.
Per BorghammerDepartment of Nuclear Medicine and PET, Aarhus University Hospital, Denmark. Electronic address: borghammer@clin.au.dk.
Kathleen L PostonDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305, USA; Department of Neurosurgery, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305, USA. Electronic address: klposton@stanford.edu.

Funding

Stanford Alzheimer's Disease Research CenterAdmin Supp: Developing iPSC models for AD and PDP30AG066515 · NIA · STANFORD UNIVERSITY · PI Victor Henderson · 2020 to 2026
$29.0M
Udall Center Director's meeting poster awardP50NS062684 · NINDS · UNIVERSITY OF WASHINGTON · PI MONTINE, THOMAS J · 2009 to 2020
$18.3M
Working Memory in Parkinson Disease: A Cognitive & Systems Neuroscience ApproachP50AG047366 · NIA · STANFORD UNIVERSITY · PI GREICIUS, MICHAEL D · 2015 to 2019
$7.9M
The impact of early Tau pathology on cognitive progression and neuropsychiatric symptoms in Parkinson's diseaseR01NS115114 · NINDS · STANFORD UNIVERSITY · PI ANDREASSON, KATRIN I., POSTON, KATHLEEN LOMBARD · 2019 to 2023
$4.2M
ENIGMA Parkinson’s Initiative: A Global Initiative for Parkinson’s DiseaseR01NS107513 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI POSTON, KATHLEEN LOMBARD, THOMPSON, PAUL M · 2021 to 2025
$3.2M
Basal Ganglia Modulation of Cognitive Systems in Parkinson's diseaseK23NS075097 · NINDS · STANFORD UNIVERSITY · PI POSTON, KATHLEEN LOMBARD · 2011 to 2015
$936k
NIA NIH HHS P30 AG066515NIA NIH HHS P50 AG047366NINDS NIH HHS K23 NS075097NINDS NIH HHS P50 NS062684NINDS NIH HHS R01 NS107513NINDS NIH HHS R01 NS115114
6 · The paper itself

Abstract

introductionTo identify clinically implementable biomarkers of cognitive impairment in Parkinson's Disease (PD) derived from resting state-functional MRI (rs-fMRI) and CSF protein analysis.

methodsIn this single-center longitudinal cohort study, we analyzed rs-fMRI and CSF biomarkers from 50 PD patients (23 cognitively normal, 18 mild cognitive impairment, 9 dementia) and 19 controls, who completed comprehensive neuropsychological testing. A subgroup of participants returned for follow-up cognitive assessments three years later. From rs-fMRI, we studied the connectivity within two distinct Default Mode Network subsystems: left-to-right hippocampus (LHC-RHC) and medial prefrontal cortex-to-posterior cingulate cortex (mPFC-PCC). We used regression analyses to determine whether imaging (LHC-RHC, mPFC-PCC), clinical (CSF Aβ-42:40, disease duration), and demographic (age, sex, education) variables were associated with global and domain-specific cognitive impairments.

resultsLHC-RHC (F

conclusionWe used biomarker techniques that are readily available in clinical and research facilities to shed light on the pathophysiologic basis of cognitive impairment in PD. Our findings suggest that there is a functionally distinct role of the hippocampal subsystem within the DMN resting state network, and that intrinsic connectivity between the hippocampi is critically related to a broad range of cognitive functions in PD.

Indexed as

Cognitive DysfunctionConnectomeParkinson DiseaseAgedAged, 80 and overAmyloid beta-PeptidesBiomarkersDefault Mode NetworkFemaleGyrus CinguliHippocampusHumansMagnetic Resonance ImagingMaleMiddle AgedPrefrontal CortexAmyloid beta-PeptidesBiomarkersBiomarkersCSFDefault mode networkDementiaMild cognitive impairmentParkinson's disease/Parkinsonismrs-fMRI

Identifiers

PMID33484978
PMCPMC7940579

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Registered trials

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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.