Evidence map›Paper›PMID 36345036›Full record

ArticleAlzheimer's research & therapy2022

Genetically predicted telomere length and Alzheimer's disease endophenotypes: a Mendelian randomization study.

Blanca Rodríguez-Fernández, Natalia Vilor-Tejedor, Eider M Arenaza-Urquijo, Gonzalo Sánchez-Benavides, Marc Suárez-Calvet, Grégory Operto, Carolina Minguillón, Karine Fauria, Gwendlyn Kollmorgen, Ivonne Suridjan and 12 more

Abstract read
In one paragraph

Article in Alzheimer's research & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed.

  1. Trial
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  7. Shorter Telomere Length in Individuals with Neurocognitive Disorder andInternational journal of molecular sciences · 2025
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  13. Review
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  16. Genetic characterization of the ALFA study: Uncovering genetic profiles in the Alzheimer's continuum.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  17. Review
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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

22 authors.

Blanca Rodríguez-Fernández *BarcelonaBeta Brain Research Center (BBRC), Pasqual Maragall Foundation, C. Wellington 30, Barcelona, 08005, Spain.
Natalia Vilor-Tejedor *BarcelonaBeta Brain Research Center (BBRC), Pasqual Maragall Foundation, C. Wellington 30, Barcelona, 08005, Spain. nvilor@barcelonabeta.org.ORCID 0000-0003-4935-6721
Eider M Arenaza-UrquijoBarcelonaBeta Brain Research Center (BBRC), Pasqual Maragall Foundation, C. Wellington 30, Barcelona, 08005, Spain.
Gonzalo Sánchez-BenavidesBarcelonaBeta Brain Research Center (BBRC), Pasqual Maragall Foundation, C. Wellington 30, Barcelona, 08005, Spain.
Marc Suárez-CalvetBarcelonaBeta Brain Research Center (BBRC), Pasqual Maragall Foundation, C. Wellington 30, Barcelona, 08005, Spain.
Grégory OpertoBarcelonaBeta Brain Research Center (BBRC), Pasqual Maragall Foundation, C. Wellington 30, Barcelona, 08005, Spain.
Carolina MinguillónBarcelonaBeta Brain Research Center (BBRC), Pasqual Maragall Foundation, C. Wellington 30, Barcelona, 08005, Spain.
Karine FauriaBarcelonaBeta Brain Research Center (BBRC), Pasqual Maragall Foundation, C. Wellington 30, Barcelona, 08005, Spain.
Gwendlyn KollmorgenRoche Diagnostics GmbH, Penzberg, Germany.
Ivonne SuridjanRoche Diagnostics International Ltd, Rotkreuz, Switzerland.
Manuel Castro de MouraJosep Carreras Leukaemia Research Institute (IJC), Badalona, Barcelona, Spain.
David PiñeyroJosep Carreras Leukaemia Research Institute (IJC), Badalona, Barcelona, Spain.
Manel EstellerJosep Carreras Leukaemia Research Institute (IJC), Badalona, Barcelona, Spain.
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, University of Gothenburg, Mölndal, Sweden.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, University of Gothenburg, Mölndal, Sweden.
Immaculata De VivoDepartment of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
José Luis MolinuevoBarcelonaBeta Brain Research Center (BBRC), Pasqual Maragall Foundation, C. Wellington 30, Barcelona, 08005, Spain.
Arcadi NavarroBarcelonaBeta Brain Research Center (BBRC), Pasqual Maragall Foundation, C. Wellington 30, Barcelona, 08005, Spain.
Juan Domingo GispertBarcelonaBeta Brain Research Center (BBRC), Pasqual Maragall Foundation, C. Wellington 30, Barcelona, 08005, Spain.
Aleix Sala-VilaBarcelonaBeta Brain Research Center (BBRC), Pasqual Maragall Foundation, C. Wellington 30, Barcelona, 08005, Spain.
Marta Crous-BouBarcelonaBeta Brain Research Center (BBRC), Pasqual Maragall Foundation, C. Wellington 30, Barcelona, 08005, Spain. marta.crous@iconcologia.net.ORCID 0000-0003-1493-4288
ALFA study

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Telomere length (TL) is associated with biological aging, consequently influencing the risk of age-related diseases such as Alzheimer's disease (AD). We aimed to evaluate the potential causal role of TL in AD endophenotypes (i.e., cognitive performance, N = 2233; brain age and AD-related signatures, N = 1134; and cerebrospinal fluid biomarkers (CSF) of AD and neurodegeneration, N = 304) through a Mendelian randomization (MR) analysis. Our analysis was conducted in the context of the ALFA (ALzheimer and FAmilies) study, a population of cognitively healthy individuals at risk of AD. A total of 20 single nucleotide polymorphisms associated with TL were used to determine the effect of TL on AD endophenotypes. Analyses were adjusted by age, sex, and years of education. Stratified analyses by APOE-ɛ4 status and polygenic risk score of AD were conducted. MR analysis revealed significant associations between genetically predicted longer TL and lower levels of CSF Aβ and higher levels of CSF NfL only in APOE-ɛ4 non-carriers. Moreover, inheriting longer TL was associated with greater cortical thickness in age and AD-related brain signatures and lower levels of CSF p-tau among individuals at a high genetic predisposition to AD. Further observational analyses are warranted to better understand these associations.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesApolipoproteins EBiomarkersEndophenotypesHumansMendelian Randomization Analysistau ProteinsTelomereAmyloid beta-PeptidesApolipoproteins EBiomarkerstau ProteinsAlzheimer’s diseaseCerebrospinal fluid biomarkersMendelian randomizationNeuroimagingPolygenic risk scoreTelomere length

Identifiers

PMID36345036
PMCPMC9641781

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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.