Evidence map›Paper›PMID 26788404›Full record

ArticleParkinson's disease2015

Association of a BACE1 Gene Polymorphism with Parkinson's Disease in a Norwegian Population.

Johannes Lange, Kristin Aaser Lunde, Camilla Sletten, Simon Geir Møller, Ole-Bjørn Tysnes, Guido Alves, Jan Petter Larsen, Jodi Maple-Grødem

Open access · goldAbstract read
In one paragraph

Article in Parkinson's disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

10 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Membrane-Targeted Quantum Dot-Based BACE1 Activity Sensors forACS applied materials & interfaces · 2024
    Article
  3. Article
  4. Review
  5. Review
  6. Article
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  8. Review
  9. Article
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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

8 authors at 4 institutions in 2 countries.

Johannes LangeThe Norwegian Centre for Movement Disorders, Stavanger University Hospital, 4011 Stavanger, Norway.
Kristin Aaser LundeThe Norwegian Centre for Movement Disorders, Stavanger University Hospital, 4011 Stavanger, Norway; Centre for Organelle Research, University of Stavanger, 4036 Stavanger, Norway.
Camilla SlettenCentre for Organelle Research, University of Stavanger, 4036 Stavanger, Norway.
Simon Geir MøllerDepartment of Biological Sciences, St. John's University, New York, NY 11439, USA.
Ole-Bjørn TysnesDepartment of Neurology, Haukeland University Hospital, 5021 Bergen, Norway; Institute for Clinical Medicine, University of Bergen, 5021 Bergen, Norway.
Guido AlvesThe Norwegian Centre for Movement Disorders, Stavanger University Hospital, 4011 Stavanger, Norway; Department of Neurology, Stavanger University Hospital, 4011 Stavanger, Norway.
Jan Petter LarsenThe Norwegian Centre for Movement Disorders, Stavanger University Hospital, 4011 Stavanger, Norway.
Jodi Maple-GrødemThe Norwegian Centre for Movement Disorders, Stavanger University Hospital, 4011 Stavanger, Norway; Centre for Organelle Research, University of Stavanger, 4036 Stavanger, Norway.
Stavanger University Hospital · NOUniversity of Stavanger · NOHaukeland University Hospital · NOSt. John's University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background. Parkinson's disease (PD) and Alzheimer's disease (AD) share pathological features, including amyloid-beta pathology. Amyloid-beta peptide is generated by sequential proteolysis of amyloid precursor protein (APP), and genetic variations in the processing pathway genes have been found to increase the risk of AD; however, the contribution in PD is unknown. Methods. The aim of this study was to investigate whether candidate polymorphisms in five genes (ADAM10, BACE1, BACE2, PSEN2, and CLU) involved in the APP processing pathway affect PD risk in a population-based cohort of patients with incident PD and control subjects from the Norwegian ParkWest study. Results. We found an association of rs638405 in BACE1 with increased risk of PD, thus providing a novel link, at the genetic level, between amyloid-beta pathology and PD.

Identifiers

PMID26788404
PMCPMC4691638
OpenAlexW2273322187

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.