Evidence map›Paper›PMID 26948379›Full record

ArticleNature communications2016

Increased amyloidogenic APP processing in APOE ɛ4-negative individuals with cerebral β-amyloidosis.

Niklas Mattsson, Philip S Insel, Sebastian Palmqvist, Erik Stomrud, Danielle van Westen, Lennart Minthon, Henrik Zetterberg, Kaj Blennow, Oskar Hansson

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

30 citing papers in PubMed, 63 citations in OpenAlex.

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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 at 5 institutions in 2 countries.

Niklas MattssonClinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Simrisbanvägen 14, Malmö 212 24, Sweden.
Philip S InselClinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Simrisbanvägen 14, Malmö 212 24, Sweden.
Sebastian PalmqvistClinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Simrisbanvägen 14, Malmö 212 24, Sweden.
Erik StomrudClinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Simrisbanvägen 14, Malmö 212 24, Sweden.
Danielle van WestenDepartment of Clinical Sciences, Diagnostic Radiology, Lund University, Box 117, Lund 221 00, Sweden.
Lennart MinthonClinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Simrisbanvägen 14, Malmö 212 24, Sweden.
Henrik ZetterbergDepartment of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London WC1N 3BG, UK.
Kaj BlennowClinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal 431 80, Sweden.
Oskar HanssonClinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Simrisbanvägen 14, Malmö 212 24, Sweden.
Lund University · SEMalmö University · SESkåne University Hospital · SEUniversity College London · GBUniversity of Gothenburg · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increased APP (amyloid precursor protein) processing causes β-amyloid (Aβ) accumulation in autosomal dominant Alzheimer's disease (AD), but it is unclear if it also affects sporadic Aβ accumulation. We tested healthy controls and patients with mild cognitive symptoms (N=331) in the BioFINDER study, using cerebrospinal fluid (CSF) Aβ40 as a surrogate for amyloidogenic APP processing. We find that levels of brain Aβ fibrils (measured by 18F-flutemetamol PET) are independently associated with high CSF Aβ40 (P<0.001) and APOE ɛ4 (P<0.001). The association between CSF Aβ40 and brain Aβ is stronger in APOE ɛ4-negative than in positive people (P=0.0080). The results are similar for CSF Aβ38 and for a combination of CSF Aβ38 and CSF Aβ40. In conclusion, sporadic Aβ accumulation may be partly associated with increased amyloidogenic APP production, especially in APOE ɛ4-negative subjects. The risk for sporadic AD may consequently depend on increased Aβ production, in addition to decreased Aβ clearance.

Indexed as

AgedAlzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAmyloidosisApolipoprotein E4BrainCerebrospinal FluidFemaleHumansMaleMiddle AgedAmyloid beta-PeptidesAmyloid beta-Protein PrecursorApolipoprotein E4

Identifiers

PMID26948379
PMCPMC4786682
OpenAlexW2299285032

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.