Evidence map›Paper›PMID 34474300›Full record

ArticleNeurobiology of aging2021

Common genetic variation is associated with longitudinal decline and network features in behavioral variant frontotemporal degeneration.

Lauren Massimo, Lior Rennert, Sharon X Xie, Christopher Olm, Jessica Bove, Vivianna Van Deerlin, David J Irwin, Murray Grossman, Corey T McMillan

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.2field-weighted citation impact, top 44% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
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  4. Differences in the soluble and insoluble proteome between primary tauopathies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    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

9 authors at 2 institutions in 1 country.

Lauren MassimoFrontotemporal Degeneration Center, Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA; School of Nursing, University of Pennsylvania, Philadelphia, PA, USA. Electronic address: lmassimo@upenn.edu.
Lior RennertDepartment of Public Health Sciences, Clemson University, Philadelphia, PA, USA. Electronic address: liorr@clemson.edu.
Sharon X XieDepartment of Biostatistics, Epidemiology and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Electronic address: sxie@pennmedicine.upenn.edu.
Christopher OlmFrontotemporal Degeneration Center, Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Electronic address: olm@pennmedicine.upenn.edu.
Jessica BoveFrontotemporal Degeneration Center, Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Electronic address: Jessica.Bove@pennmedicine.upenn.edu.
Vivianna Van DeerlinDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
David J IrwinFrontotemporal Degeneration Center, Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Electronic address: dirwin@pennmedicine.upenn.edu.
Murray GrossmanFrontotemporal Degeneration Center, Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Electronic address: mgrossma@pennmedicine.upenn.edu.
Corey T McMillanFrontotemporal Degeneration Center, Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Electronic address: mcmillac@pennmedicine.upenn.edu.
University of Pennsylvania · USClemson University · US

Funding

Transgenic Mouse Models of Tau PathologiesP01AG017586 · NIA · UNIVERSITY OF PENNSYLVANIA · PI LEE, VIRGINIA M · 2000 to 2021
$37.3M
Research Education ComponentP30AG072979 · NIA · UNIVERSITY OF PENNSYLVANIA · PI DAVID A WOLK · 2021 to 2026
$24.8M
Understanding Environmental Contributions to Heterogeneity in bvFTD.P01AG066597 · NIA · UNIVERSITY OF PENNSYLVANIA · PI David John Irwin, Corey T McMillan · 2020 to 2026
$18.8M
Connectomic imaging in familial and sporadic frontotemporal degenerationU01AG052943 · NIA · UNIVERSITY OF PENNSYLVANIA · PI GORNO TEMPINI, MARIA LUISA, GROSSMAN, MURRAY · 2016 to 2019
$5.9M
Microscopic and Large-Scale Networks of Molecular Pathology in Frontotemporal Lobar DegenerationR01NS109260 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI IRWIN, DAVID JOHN · 2019 to 2023
$3.8M
Cognitive and Neural Moderators of Longitudinal Decline in Frontotemporal DegenerationR00AG056054 · NIA · UNIVERSITY OF PENNSYLVANIA · PI MASSIMO, LAUREN M · 2018 to 2020
$747k
Cognitive and Neural Moderators of Longitudinal Decline in Frontotemporal DegenerationK99AG056054 · NIA · PENNSYLVANIA STATE UNIVERSITY, THE · PI MASSIMO, LAUREN M · 2016 to 2017
$192k
NIA NIH HHS K99 AG056054NIA NIH HHS P01 AG017586NIA NIH HHS P01 AG066597NIA NIH HHS P30 AG072979NIA NIH HHS R00 AG056054NIA NIH HHS U01 AG052943NINDS NIH HHS R01 NS109260
6 · The paper itself

Abstract

The T allele in rs1768208 located in or near the myelin oligodendrocyte basic protein gene (MOBP) is a risk factor for frontotemporal degeneration pathology. We evaluated the hypothesis that the presence of a T allele in rs1768208 will be associated with rate of cognitive decline in behavioral variant frontotemporal degeneration (bvFTD) related to compromised frontal networks. We studied 81 individuals clinically diagnosed with bvFTD who were genotyped for rs1768208 and coded using a dominant model reflecting the presence (i.e., MOBP +) or absence (MOBP -) of the T risk allele. Linear mixed-effects models assessed the association of genotype on neuropsychological performance over time. Regression analyses examined differences in network structure by MOBP genotype. We found a genotype by time interaction for declining cognitive performance, whereby MOBP + individuals demonstrated faster rates of decline in executive function. The presence of a MOBP risk allele was associated with degradation of white matter network features in the frontal lobe. These findings suggest that individual genetic variation may contribute to heterogeneity in clinical progression.

Indexed as

Genetic Association StudiesPolymorphism, Single NucleotideAgedAllelesBrainCognitionExecutive FunctionFemaleFrontotemporal DementiaGenotypeHumansMagnetic Resonance ImagingMaleMiddle AgedMyelin ProteinsNeuroimagingMOBP protein, humanMyelin ProteinsFrontotemporal degenerationlongitudinal declineMOBPMRI

Identifiers

PMID34474300
PMCPMC8616801
OpenAlexW3188090963

What OpenQuestion holds

Textmetadata
LicenceTDM
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.