Evidence map›Paper›PMID 36815874›Full record

ArticleAlzheimer's & dementia (Amsterdam, Netherlands)

Endo-lysosomal protein concentrations in CSF from patients with frontotemporal dementia caused by

Anders Toft, Simon Sjödin, Anja Hviid Simonsen, Patrick Ejlerskov, Peter Roos, Christian Sandøe Musaeus, Emil Elbæk Henriksen, Troels Tolstrup Nielsen, Ann Brinkmalm, Kaj Blennow and 2 more

Open access · goldAbstract read
In one paragraph

Article in Alzheimer's & dementia (Amsterdam, Netherlands). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
0.4field-weighted citation impact, top 42% 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

4 citing papers in PubMed, 1 synthesis or guideline pooled it, 2 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
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

12 authors at 4 institutions in 3 countries.

Anders ToftNeurogenetics Clinic & Research Lab Danish Dementia Research Centre Rigshospitalet Copenhagen Denmark.
Simon SjödinLaboratory of Clinical Chemistry Sahlgrenska University Hospital Gothenburg Sweden.
Anja Hviid SimonsenNeurogenetics Clinic & Research Lab Danish Dementia Research Centre Rigshospitalet Copenhagen Denmark.
Patrick EjlerskovNeurogenetics Clinic & Research Lab Danish Dementia Research Centre Rigshospitalet Copenhagen Denmark.
Peter RoosNeurogenetics Clinic & Research Lab Danish Dementia Research Centre Rigshospitalet Copenhagen Denmark.
Christian Sandøe MusaeusNeurogenetics Clinic & Research Lab Danish Dementia Research Centre Rigshospitalet Copenhagen Denmark.
Emil Elbæk HenriksenNeurogenetics Clinic & Research Lab Danish Dementia Research Centre Rigshospitalet Copenhagen Denmark.
Troels Tolstrup NielsenNeurogenetics Clinic & Research Lab Danish Dementia Research Centre Rigshospitalet Copenhagen Denmark.
Ann BrinkmalmClinical Neurochemistry Laboratory Sahlgrenska University Hospital Mölndal Sweden.
Kaj BlennowClinical Neurochemistry Laboratory Sahlgrenska University Hospital Mölndal Sweden.
Henrik ZetterbergClinical Neurochemistry Laboratory Sahlgrenska University Hospital Mölndal Sweden.
Jørgen Erik NielsenNeurogenetics Clinic & Research Lab Danish Dementia Research Centre Rigshospitalet Copenhagen Denmark.
Rigshospitalet · DKSahlgrenska University Hospital · SENational Hospital for Neurology and Neurosurgery · GBUniversity of Gothenburg · SE

Funding

The effects of iron on oxidative stress and Alzheimer's biomarkers in amyloid-positive and negative elderly normalR01AG068398 · NIA · WEILL MEDICAL COLL OF CORNELL UNIV · PI CHIANG, GLORIA CHIA-YI · 2020 to 2024
$2.8M
NIA NIH HHS R01 AG068398
6 · The paper itself

Abstract

Introduction: Increasing evidence implicates proteostatic dysfunction as an early event in the development of frontotemporal dementia (FTD). This study aimed to explore potential cerebrospinal fluid (CSF) biomarkers associated with the proteolytic systems in genetic FTD caused by Methods: Combining solid-phase extraction and parallel reaction monitoring mass spectrometry, a panel of 47 peptides derived from 20 proteins was analyzed in CSF from 31 members of the Danish Results: Compared with family controls, mutation carriers had significantly higher levels of complement C9, lysozyme and transcobalamin II, and lower levels of ubiquitin, cathepsin B, and amyloid precursor protein. Discussion: Lower CSF ubiquitin concentrations in Highlights: CSF markers of proteostasis were explored in

Indexed as

amyloid precursor proteinbiomarkerscathepsin Bcerebrospinal fluidcomplement C9frontotemporal dementialysozymeproteomicstranscobalamin IIubiquitin

Identifiers

PMID36815874
PMCPMC9936136
OpenAlexW4321236054

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.