Evidence map›Paper›PMID 24179803›Full record

ArticleNeuroImage. Clinical2013

Polymorphism of brain derived neurotrophic factor influences β amyloid load in cognitively intact apolipoprotein E ε4 carriers.

Katarzyna Adamczuk, An-Sofie De Weer, Natalie Nelissen, Kewei Chen, Kristel Sleegers, Karolien Bettens, Christine Van Broeckhoven, Mathieu Vandenbulcke, Pradeep Thiyyagura, Patrick Dupont and 3 more

2 registry-linked trialsOpen access · goldAbstract read
In one paragraph

Article in NeuroImage. Clinical, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.2field-weighted citation impact, top 13% 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.

NCT02778971 completednot on this mapstarted 2016, after this paper: background citation

Implications for Management of PET Amyloid Classification Technology

TypeobservationalSponsorUniversity of UtahRan2016 to 2022Enrolled41ConditionsMild Cognitive Impairment, Dementia, Alzheimer's DiseaseArms[18F]Flutemetamol
NCT02781220 terminatednot on this mapstarted 2016, after this paper: background citation

Implications for Management of PET Amyloid Classification Technology in the Imaging Dementia(IDEAS) Trial

TypeobservationalSponsorUniversity of UtahRan2016 to 2023Enrolled69ConditionsMild Cognitive Impairment, Dementia, Alzheimer's Disease
3 · Its place in the literature

Who cites it

36 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
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  12. Lack of association between bridging integrator 1 (Alzheimer's & dementia (New York, N. Y.) · 2022
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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

13 authors at 6 institutions in 2 countries.

Katarzyna AdamczukLaboratory for Cognitive Neurology, University of Leuven, Belgium ; Alzheimer Research Centre KU Leuven, Leuven Institute for Neuroscience and Disease, Belgium.
An-Sofie De Weer
Natalie Nelissen
Kewei Chen
Kristel Sleegers
Karolien Bettens
Christine Van Broeckhoven
Mathieu Vandenbulcke
Pradeep Thiyyagura
Patrick Dupont
Koen Van Laere
Eric M Reiman
Rik Vandenberghe
KU Leuven · BEVIB-KU Leuven Center for Brain & Disease Research · BEArizona Alzheimer’s ConsortiumVIB-UAntwerp Center for Molecular Neurology · BEAlzheimer's Association · USUniversity of Antwerp · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aside from apolipoprotein E (APOE), genetic risk factors for β amyloid deposition in cognitively intact individuals remain to be identified. Brain derived neurotrophic factor (BDNF) modulates neural plasticity, which has been implicated in Alzheimer's disease. We examined in cognitively normal older adults whether the BDNF codon 66 polymorphism affects β amyloid burden and the relationship between β amyloid burden and cognitive scores, and how this relates to the effect of APOE. Amyloid load was measured by means of (18)F-flutemetamol PET in 64 community-recruited cognitively intact individuals (mean age 66, S.D. 5.1). Recruitment was stratified according to a factorial design with APOE (ε4 allele present vs absent) and BDNF (met allele at codon 66 present vs absent) as factors. Individuals in the four resulting cells were matched by the number of cases, age, and gender. Among the APOE ε4 carriers, BDNF met positive subjects had a significantly higher amyloid load than BDNF met negative subjects, while BDNF met carrier status did not have an effect in APOE ε4 noncarriers. This interaction effect was localized to precuneus, orbitofrontal cortex, gyrus rectus, and lateral prefrontal cortex. In the APOE ε4/BDNF met carriers, a significant inverse relationship existed between episodic memory scores and amyloid burden but not in any of the other groups. This hypothesis-generating experiment highlights a potential role of BDNF polymorphisms in the preclinical phase of β amyloid deposition and also suggests that BDNF codon 66 polymorphisms may influence resilience against β amyloid-related effects on cognition.

Indexed as

AD, Alzheimer's diseaseAlzheimerAmyloid PETAPOEAPOE, apolipoprotein EBDNFBDNF, brain-derived neurotrophic factorFlutemetamolmet, methionineMRI, magnetic resonance imagingPET, positron emission tomographyPVC, partial volume correctionSUVRcomp, SUVR in composite cortical volume of interestSUVR, standardized uptake value ratioval, valineVOI, volume-of-interest

Identifiers

PMID24179803
PMCPMC3777754
OpenAlexW2144503366

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

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.