Evidence map›Paper›PMID 24252417›Full record

ArticleActa neuropathologica communications2013

CSF Presenilin-1 complexes are increased in Alzheimer's disease.

María-Salud García-Ayllón, María-Letizia Campanari, Gunnar Brinkmalm, Alberto Rábano, Jordi Alom, Carlos A Saura, Niels Andreasen, Kaj Blennow, Javier Sáez-Valero

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

20 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Biomarkers for Alzheimer's Disease Early Diagnosis.Journal of personalized medicine · 2020
    Review
  9. Article
  10. TheFrontiers in neuroscience · 2019
    Article
  11. PeerJ · 2019
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. CSF beta-amyloid 1-42 - what are we measuring in Alzheimer's disease?Annals of clinical and translational neurology · 2015
    Article
  19. Article
  20. 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 6 institutions in 2 countries.

María-Salud García-AyllónInstituto de Neurociencias de Alicante, Universidad Miguel Hernández-CSIC, Av, Ramón y Cajal s/n, Sant Joan d'Alacant E-03550, Spain. j.saez@umh.es.
María-Letizia Campanari
Gunnar Brinkmalm
Alberto Rábano
Jordi Alom
Carlos A Saura
Niels Andreasen
Kaj Blennow
Javier Sáez-Valero
Instituto de Neurociencias · ESUniversity of Gothenburg · SEBiomedical Research Networking Center on Neurodegenerative Diseases · ESFundacion Centro De Investigacion De Enfermedades Neurologicas · ESKarolinska Institutet · SEUniversitat Autònoma de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPresenilin-1 (PS1) is the active component of the amyloid precursor protein cleaving γ-secretase complex. PS1 protein is a transmembrane protein containing multiple hydrophobic regions which presence in cerebrospinal fluid (CSF) has not been measured to date. This study assesses whether PS1 and other components of the γ-secretase complex are present in CSF.

resultsHere, we show that PS1 is present in ventricular post-mortem and lumbar ante-mortem CSF, and plasma as 100-150-kDa hetero-complexes containing both the N- and C-terminal fragments (NTF and CTF) of the protein. Immunoprecipitation and immunoblotting with different antibodies confirmed the identity of the PS1 species. The γ-secretase components, APH-1 (anterior pharynx-defective 1) and PEN-2 (presenilin enhancer 2), as well as presenilin-2 (PS2) fragments, co-exist within these CSF complexes, while nicastrin is not detected. These CSF-PS1 complexes differ from active γ-secretase membrane-complexes, and may represent nonspecific aggregation of the PS1 protein. Levels of PS1 complexes are increased in CSF samples from autopsy-confirmed Alzheimer's disease (AD) cases and were found to be more stable than complexes in CSF from control subjects. Despite similar levels of total PS1 in CSF from probable AD patients and cognitively normal subjects, an increased proportion of highly stable PS1 complexes were observed in AD CSF.

conclusionsOur data suggest that fragments of the PS1 protein present in CSF as complexes may be useful as a biomarker for AD.

Indexed as

AgedAlzheimer DiseaseAmyloid Precursor Protein SecretasesAnimalsAspartic Acid EndopeptidasesBiomarkersEndopeptidasesFemaleHumansImmunoblottingImmunoprecipitationLumbar VertebraeMaleMembrane ProteinsMice, Inbred C57BLMice, KnockoutAmyloid Precursor Protein SecretasesAPH1A protein, humanAspartic Acid EndopeptidasesBACE1 protein, humanBiomarkersEndopeptidasesMembrane ProteinsPeptide HydrolasesPresenilin-1presenilin 1, mousePSEN1 protein, humanPSENEN protein, human

Identifiers

PMID24252417
PMCPMC3893612
OpenAlexW2131120955

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LicenceCC BY
Read underepoch 390

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.