Evidence map›Paper›PMID 27653981›Full record

ArticleBrain research2016

Cerebrospinal fluid-induced retardation of amyloid β aggregation correlates with Alzheimer's disease and the APOE ε4 allele.

E R Padayachee, H Zetterberg, E Portelius, J Borén, J L Molinuevo, N Andreasen, R Cukalevski, S Linse, K Blennow, U Andreasson

Open access · hybridAbstract read
In one paragraph

Article in Brain research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

14 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Apolipoprotein E particle size is increased in Alzheimer's disease.Alzheimer's & dementia (Amsterdam, Netherlands) · 2019
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Ultrasensitive Measurement of CaAngewandte Chemie (International ed. in English) · 2017
    Article
  14. Systematic development of small molecules to inhibit specific microscopic steps of Aβ42 aggregation in Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2017
    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

10 authors at 5 institutions in 3 countries.

E R PadayacheeClinical Neurochemistry Lab, Inst. of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden. Electronic address: padayachee.eden@gmail.com.
H ZetterbergClinical Neurochemistry Lab, Inst. of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden; Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom.
E PorteliusClinical Neurochemistry Lab, Inst. of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden.
J BorénWallenberg Laboratory, Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden.
J L MolinuevoAlzheimer's Disease and Other Cognitive Disorders Unit, Neurology Service, ICN Hospital Clinic i Universitari and Pasqual Maragall Foundation, Barcelona, Spain.
N AndreasenDepartment of Geriatrics, Karolinska University Hospital, Stockholm, Sweden.
R CukalevskiDepartment of Biochemistry and Structural Biology, Lund University, Lund, Sweden.
S LinseDepartment of Biochemistry and Structural Biology, Lund University, Lund, Sweden.
K BlennowClinical Neurochemistry Lab, Inst. of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden.
U AndreassonClinical Neurochemistry Lab, Inst. of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden.
University of Gothenburg · SELund University · SEKarolinska University Hospital · SEPasqual Maragall Foundation · ESUniversity College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Misfolding and aggregation of amyloid β (Aβ) are key features of Alzheimer's disease (AD) pathogenesis, but the molecular events controlling this process are not known in detail. In vivo, Aβ aggregation and plaque formation occur in the interstitial fluid of the brain extracellular matrix. This fluid communicates freely with cerebrospinal fluid (CSF). Here, we examined the effect of human CSF on Aβ aggregation kinetics in relation to AD diagnosis and carrier status of the apolipoprotein E (APOE) ε4 allele, the main genetic risk factor for sporadic AD. The aggregation of Aβ was inhibited in the presence of CSF and, surprisingly, the effect was more pronounced in APOE ε4 carriers. However, by fractionation of CSF using size exclusion chromatography, it became evident that it was not the ApoE protein itself that conveyed the inhibition, since the retarding species eluted at lower volume, corresponding to a much higher molecular weight, than ApoE monomers. Cholesterol quantification and immunoblotting identified high-density lipoprotein particles in the retarding fractions, indicating that such particles may be responsible for the inhibition. These results add information to the yet unresolved puzzle on how the risk factor of APOE ε4 functions in AD pathogenesis.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesApolipoprotein E4BenzothiazolesCase-Control StudiesCerebrospinal FluidCholesterol, HDLChromatography, GelFemaleHeterozygoteHumansImmunoblottingKineticsMaleAmyloid beta-Peptidesamyloid beta-protein (1-42)Apolipoprotein E4BenzothiazolesCholesterol, HDLPeptide FragmentsThiazolesthioflavin TAggregationAmyloid-βApolipoprotein ε4CholesterolHigh density lipoproteinsInhibitionKineticsNeurofibrillary tanglesThioflavin T

Identifiers

PMID27653981
PMCPMC5090044
OpenAlexW2523519098

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.