Evidence map›Paper›PMID 32080211›Full record

ArticleScientific reports2020

Mid age APOE ε4 carriers show memory-related functional differences and disrupted structure-function relationships in hippocampal regions.

Simon L Evans, Nicholas G Dowell, Fenella Prowse, Naji Tabet, Sarah L King, Jennifer M Rusted

Abstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

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  5. A Review of the Current Status of Disease-Modifying Therapies and Prevention of Alzheimer's Disease.Medical science monitor : international medical journal of experimental and clinical research · 2024
    Review
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  7. International journal of molecular sciences · 2023
    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

6 authors.

Simon L EvansSchool of Psychology and Sussex Neuroscience, University of Sussex, Brighton, East Sussex, BN1 9QG, United Kingdom.ORCID http://orcid.org/0000-0001-7875-9445
Nicholas G DowellClinical Imaging Sciences Centre, Brighton and Sussex Medical School, Brighton, East Sussex, BN1 9RR, United Kingdom.
Fenella ProwseBrighton and Sussex Medical School (BSMS), Brighton, East Sussex, BN1 9RN, United Kingdom.
Naji TabetCentre for Dementia Studies, Brighton and Sussex Medical School, Brighton, East Sussex, BN1 9RN, United Kingdom.
Sarah L KingSchool of Psychology and Sussex Neuroscience, University of Sussex, Brighton, East Sussex, BN1 9QG, United Kingdom.
Jennifer M RustedSchool of Psychology and Sussex Neuroscience, University of Sussex, Brighton, East Sussex, BN1 9QG, United Kingdom. j.rusted@sussex.ac.uk.

Funding

Biotechnology and Biological Sciences Research Council BB/L009242/1
6 · The paper itself

Abstract

Carriers of the APOE e4 allele are at higher risk of age-related cognitive decline and Alzheimer's disease (AD). The underlying neural mechanisms are uncertain, but genotype differences in medial temporal lobe (MTL) functional activity and structure at mid-age might contribute. We tested 16 non-e4 and 16 e4 carriers (aged 45-55) on a subsequent memory task in conjunction with MRI to assess how hippocampal volume (from T1 structural) and microstructure (neurite orientation-dispersion, from NODDI) differs by genotype and in relation to memory encoding. No previous study has investigated APOE effects on hippocampal microstructure using NODDI. Recall performance did not differ by genotype. A genotype by condition interaction in left parahippocampus indicated that in e4 carriers activity did not differentiate subsequently remembered from forgotten words. Hippocampal volumes and microstructure also did not differ by genotype but hippocampal volumes correlated positively with recognition performance in non-e4 carriers only. Similarly, greater hippocampal neurite orientation-dispersion was linked to better recall but only in non-e4s. Thus, we suggest that mid-age e4 carriers show a breakdown of normal MTL activation and structure-performance relationships. This could reflect an inability to utilise compensatory mechanisms, and contribute to higher risk of cognitive decline and AD in later life.

Indexed as

HeterozygoteAgingAllelesApolipoprotein E4Brain MappingCognition DisordersFemaleGenotypeHippocampusHumansImage Processing, Computer-AssistedMagnetic Resonance ImagingMaleMemoryMiddle AgedNeuritesApolipoprotein E4

Identifiers

PMID32080211
PMCPMC7033211

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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.