Evidence map›Paper›PMID 30390709›Full record

ArticleActa neuropathologica communications2018

Variation in TMEM106B in chronic traumatic encephalopathy.

Jonathan D Cherry, Jesse Mez, John F Crary, Yorghos Tripodis, Victor E Alvarez, Ian Mahar, Bertrand R Huber, Michael L Alosco, Raymond Nicks, Bobak Abdolmohammadi and 17 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta neuropathologica communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

45 citing papers in PubMed, 62 citations in OpenAlex.

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  17. A common Alu insertion in the 3'UTR of TMEM106B is associated with risk of dementia.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
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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

27 authors at 3 institutions in 3 countries.

Jonathan D CherryBoston University Alzheimer's Disease and CTE Center, Boston University School of Medicine, 72 E Concord Street, B7800, Boston, MA, 02118, USA.
Jesse MezBoston University Alzheimer's Disease and CTE Center, Boston University School of Medicine, 72 E Concord Street, B7800, Boston, MA, 02118, USA.
John F CraryDepartment of Pathology, Fishberg Department of Neuroscience, Friedman Brain Institute, Ronald M. Loeb Center for Alzheimer's Disease, Icahn School of Medicine at Mount Sinai School, New York, NY, 10029, USA.
Yorghos TripodisDepartment of Biostatistics, Boston University School of Public Health, Boston, MA, 20118, USA.
Victor E AlvarezBoston University Alzheimer's Disease and CTE Center, Boston University School of Medicine, 72 E Concord Street, B7800, Boston, MA, 02118, USA.
Ian MaharBoston University Alzheimer's Disease and CTE Center, Boston University School of Medicine, 72 E Concord Street, B7800, Boston, MA, 02118, USA.
Bertrand R HuberBoston University Alzheimer's Disease and CTE Center, Boston University School of Medicine, 72 E Concord Street, B7800, Boston, MA, 02118, USA.
Michael L AloscoBoston University Alzheimer's Disease and CTE Center, Boston University School of Medicine, 72 E Concord Street, B7800, Boston, MA, 02118, USA.
Raymond NicksDepartment of Veterans Affairs Medical Center, Bedford, MA, 01730, USA.
Bobak AbdolmohammadiBoston University Alzheimer's Disease and CTE Center, Boston University School of Medicine, 72 E Concord Street, B7800, Boston, MA, 02118, USA.
Patrick T KiernanBoston University Alzheimer's Disease and CTE Center, Boston University School of Medicine, 72 E Concord Street, B7800, Boston, MA, 02118, USA.
Laney EversBoston University Alzheimer's Disease and CTE Center, Boston University School of Medicine, 72 E Concord Street, B7800, Boston, MA, 02118, USA.
Sarah SvirskyBoston University Alzheimer's Disease and CTE Center, Boston University School of Medicine, 72 E Concord Street, B7800, Boston, MA, 02118, USA.
Katharine BabcockBoston University Alzheimer's Disease and CTE Center, Boston University School of Medicine, 72 E Concord Street, B7800, Boston, MA, 02118, USA.
Hannah M GardnerVA Boston Healthcare System, 150 S. Huntington Avenue, Boston, MA, 02130, USA.
Gaoyuan MengVA Boston Healthcare System, 150 S. Huntington Avenue, Boston, MA, 02130, USA.
Christopher J NowinskiBoston University Alzheimer's Disease and CTE Center, Boston University School of Medicine, 72 E Concord Street, B7800, Boston, MA, 02118, USA.
Brett M MartinDepartment of Biostatistics, Boston University School of Public Health, Boston, MA, 20118, USA.
Brigid DwyerDepartment of Neurology, Boston University School of Medicine, 72 E Concord Street, B7800, Boston, MA, 20118, USA.
Neil W KowallBoston University Alzheimer's Disease and CTE Center, Boston University School of Medicine, 72 E Concord Street, B7800, Boston, MA, 02118, USA.
Robert C CantuDepartment of Anatomy and Neurobiology, Boston University School of Medicine, Boston, MA, 20119, USA.
Lee E GoldsteinBoston University Alzheimer's Disease and CTE Center, Boston University School of Medicine, 72 E Concord Street, B7800, Boston, MA, 02118, USA.
Douglas I KatzDepartment of Neurology, Boston University School of Medicine, 72 E Concord Street, B7800, Boston, MA, 20118, USA.
Robert A SternBoston University Alzheimer's Disease and CTE Center, Boston University School of Medicine, 72 E Concord Street, B7800, Boston, MA, 02118, USA.
Lindsay A FarrerDepartment of Neurology, Boston University School of Medicine, 72 E Concord Street, B7800, Boston, MA, 20118, USA.
Ann C McKeeBoston University Alzheimer's Disease and CTE Center, Boston University School of Medicine, 72 E Concord Street, B7800, Boston, MA, 02118, USA. amckee@bu.edu.
Thor D SteinBoston University Alzheimer's Disease and CTE Center, Boston University School of Medicine, 72 E Concord Street, B7800, Boston, MA, 02118, USA. tdstein@bu.edu.ORCID 0000-0001-6954-4477
Boston University · USVA Boston Healthcare System · USAllen Institute for Brain Science · US

Funding

Neuropathology CoreP30AG013846 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI KOWALL, NEIL W. · 1996 to 2020
$29.1M
Chronic Traumatic Encephalopathy: Detection, Diagnosis, Course, and Risk FactorsU01NS093334 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI CUMMINGS, JEFFREY L., REIMAN, ERIC MICHAEL · 2016 to 2022
$17.0M
CTE and Posttraumatic Neurodegeneration: Neuropathology and Ex Vivo ImagingU01NS086659 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MCKEE, ANN C. · 2014 to 2017
$6.1M
The Contribution of Age-Related Taupahtoies to Alzheimer's Disease-SupplementR01AG062348 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI CRARY, JOHN FONDA, DICKSON, DENNIS WILLIAM · 2018 to 2022
$4.5M
Tau Pathology in CTE vs. Alzheimer's Disease: Microvasculopathy and NeuroinflammationRF1AG057902 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MCKEE, ANN C. · 2017 to 2017
$4.1M
Epigenetic changes in synaptic and inflammatory genes involved in the age-dependent development of Alzheimer's disease pathologies andcognitive declineRF1AG054156 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI AU, RHODA, RYU, HOON · 2016 to 2018
$3.4M
Chronic Traumatic Encephalopathy: Clinical Presentation and BiomarkersR01NS078337 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI STERN, ROBERT A · 2011 to 2013
$2.0M
Age-Associated Lipidomic Changes in Alzheimer's DiseaseR56AG057768 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI BLUSZTAJN, JAN KRZYSZTOF, STEIN, THOR · 2017 to 2017
$820k
Repetitive Head Impact Exposure and Later-Life White Matter Signal Abnormalities: An Investigation in Former NFL Players, Subjects with Alzheimer's Disease, and Cognitively Normal ControlsK23NS102399 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI ALOSCO, MICHAEL · 2018 to 2022
$793k
Chronic Traumatic Encephalopathy: Clinical Presentation and BiomarkersR56NS078337 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI STERN, ROBERT A · 2014 to 2014
$786k
Genetic and Neuropsychological Heterogeneity in Alzheimer's DiseaseK23AG046377 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MEZ, JESSE BENJAMIN · 2014 to 2018
$639k
VA Biorepository Brain BankI01BX002466 · VA · VA BOSTON HEALTH CARE SYSTEM · PI Ann C. McKee, Haining Zhu · 2014 to 2026
–
BLRD VA I01 BX002466CSRD VA I01 CX001038CSRD VA I01 CX001135NIA NIH HHS K23 AG046377NIA NIH HHS P30 AG013846NIA NIH HHS R01 AG062348NIA NIH HHS R56 AG057768NIA NIH HHS RF1 AG054156NIA NIH HHS RF1 AG057902NINDS NIH HHS K23 NS102399NINDS NIH HHS R01 NS078337NINDS NIH HHS R56 NS078337NINDS NIH HHS U01 NS086659NINDS NIH HHS U01 NS093334
6 · The paper itself

Abstract

The genetic basis of chronic traumatic encephalopathy (CTE) is poorly understood. Variation in transmembrane protein 106B (TMEM106B) has been associated with enhanced neuroinflammation during aging and with TDP-43-related neurodegenerative disease, and rs3173615, a missense coding SNP in TMEM106B, has been implicated as a functional variant in these processes. Neuroinflammation and TDP-43 pathology are prominent features in CTE. The purpose of this study was to determine whether genetic variation in TMEM106B is associated with CTE risk, pathological features, and ante-mortem dementia. Eighty-six deceased male athletes with a history of participation in American football, informant-reported Caucasian, and a positive postmortem diagnosis of CTE without comorbid neurodegenerative disease were genotyped for rs3173615. The minor allele frequency (MAF = 0.42) in participants with CTE did not differ from previously reported neurologically normal controls (MAF = 0.43). However, in a case-only analysis among CTE cases, the minor allele was associated with reduced phosphorylated tau (ptau) pathology in the dorsolateral frontal cortex (DLFC) (AT8 density, odds ratio [OR] of increasing one quartile = 0.42, 95% confidence interval [CI] 0.22-0.79, p = 0.008), reduced neuroinflammation in the DLFC (CD68 density, OR of increasing one quartile = 0.53, 95% CI 0.29-0.98, p = 0.043), and increased synaptic protein density (β = 0.306, 95% CI 0.065-0.546, p = 0.014). Among CTE cases, TMEM106B minor allele was also associated with reduced ante-mortem dementia (OR = 0.40, 95% CI 0.16-0.99, p = 0.048), but was not associated with TDP-43 pathology. All case-only models were adjusted for age at death and duration of football play. Taken together, variation in TMEM106B may have a protective effect on CTE-related outcomes.

Indexed as

AdolescentAdultAgedAged, 80 and overAmyloid beta-PeptidesAntigens, CDAntigens, Differentiation, MyelomonocyticCD68 MoleculeChronic Traumatic EncephalopathyDisks Large Homolog 4 ProteinFootballGenotypeHumansLinkage DisequilibriumMaleMembrane ProteinsAmyloid beta-PeptidesAntigens, CDAntigens, Differentiation, MyelomonocyticCD68 antigen, humanCD68 MoleculeDisks Large Homolog 4 ProteinDLG4 protein, humanMembrane ProteinsNerve Tissue Proteinstau ProteinsTMEM106B protein, humanChronic traumatic encephalopathyDementiaFootballGeneticsNeuroinflammationTauTDP-43TMEM106BTraumatic brain injury

Identifiers

PMID30390709
PMCPMC6215686
OpenAlexW2899509891

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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.