Evidence map›Paper›PMID 35864212›Full record

ArticleJournal of neurology2022

A longitudinal

Min Chu, Zhongyun Chen, Binbin Nie, Li Liu, Kexin Xie, Yue Cui, Kewei Chen, Pedro Rosa-Neto, Liyong Wu

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neurology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 45% of its field
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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Review
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 at 4 institutions in 3 countries.

Min ChuDepartment of Neurology, Xuanwu Hospital, Capital Medical University, Changchun Street 45, Beijing, 100053, China.
Zhongyun ChenDepartment of Neurology, Xuanwu Hospital, Capital Medical University, Changchun Street 45, Beijing, 100053, China.
Binbin NieBeijing Engineering Research Center of Radiographic Techniques and Equipment, Institute of High Energy Physics, Chinese Academy of Sciences, Beijing, China.
Li LiuDepartment of Neurology, Xuanwu Hospital, Capital Medical University, Changchun Street 45, Beijing, 100053, China.
Kexin XieDepartment of Neurology, Xuanwu Hospital, Capital Medical University, Changchun Street 45, Beijing, 100053, China.
Yue CuiDepartment of Neurology, Xuanwu Hospital, Capital Medical University, Changchun Street 45, Beijing, 100053, China.
Kewei ChenBanner Alzheimer's Institute, Phoenix, AZ, USA.
Pedro Rosa-NetoAlzheimer's Disease Research Unit, McGill Centre for Studies in Aging, Montreal, H4H 1R3, Canada.
Liyong WuDepartment of Neurology, Xuanwu Hospital, Capital Medical University, Changchun Street 45, Beijing, 100053, China. wmywly@hotmail.com.
Capital Medical University · CNArizona State University · USChinese Academy of Sciences · CNMcGill University Health Centre · CA

Funding

Research Education ComponentP30AG019610 · NIA · SUN HEALTH RESEARCH INSTITUTE · PI REIMAN, ERIC MICHAEL · 2001 to 2020
$32.5M
Research Education ComponentP30AG072980 · NIA · BANNER HEALTH · PI Nicholas Ashton · 2021 to 2026
$24.9M
NIA NIH HHS P30 AG019610NIA NIH HHS P30 AG072980
6 · The paper itself

Abstract

backgroundPathogenic prion protein may start to deposit in some brain regions and cause functional alterations in the asymptomatic stage in Creutzfeldt-Jakob disease. The study aims to determine the trajectory of the brain metabolic changes for prion protein diseases at the preclinical stage.

methodsAt baseline, we enrolled five asymptomatic PRNP G114V mutation carriers, six affected genetic PRNP E200K CJD patients and 23 normal controls. All participants completed clinical, diffusion-weighted imaging (DWI) and

resultsAt baseline, DWI signals, the cerebral glucose standardized uptake value rate ratio (SUVR) and clinical status in 5 asymptomatic cases were normal. At the follow-up period, mild hypometabolism on PET images was found in asymptomatic carriers without any DWI abnormal signal. Further group quantitatively analysis showed hypometabolic brain regions in the asymptomatic genetic CJD group were in the insula, frontal, parietal, and temporal lobes in 4-year follow-up. The SUVR changing trajectories of all asymptomatic cases were within the range between the normal controls and affected patients. Notably, the SUVR of one asymptomatic individual whose baseline age was older showed a rapid decline at the last follow-up.

conclusionsOur study illustrates that the neurodegenerative process associated with genetic CJD may initiate before the clinical presentation of the disease.

Indexed as

Creutzfeldt-Jakob SyndromeFluorodeoxyglucose F18BrainGlucoseHumansMagnetic Resonance ImagingMutationPositron-Emission TomographyPrion ProteinsFluorodeoxyglucose F18GlucosePrion Proteins18F fluorodeoxyglucose-positron emission tomographyAsymptomatic stageDiffusion-weighted imagingGenetic Creutzfeldt–Jakob disease

Identifiers

PMID35864212
PMCPMC9553814
OpenAlexW4286203204

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.