Loss of Tmem106b is unable to ameliorate frontotemporal dementia-like phenotypes in an AAV mouse model of C9ORF72-repeat induced toxicity.

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.

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.

Who cites it

19 citing papers in PubMed, 23 citations in OpenAlex.

1. Divergent and convergent TMEM106B pathology in murine models of neurodegeneration and human disease.Acta neuropathologica communications · 2025
   Article
2. Dysregulated Expression of Inflammasome and Extracellular Matrix Genes inASN neuro · 2025
   Article
3. The role of autophagy in the pathogenesis and treatment of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).Autophagy reports · 2025
   Review
4. TMEM106B coding variant is protective and deletion detrimental in a mouse model of tauopathy.Acta neuropathologica · 2024
   Article
5. The endolysosomal pathway and ALS/FTD.Trends in neurosciences · 2023
   Review
6. Superresolution live-cell imaging reveals that the localization of TMEM106B to filopodia in oligodendrocytes is compromised by the hypomyelination-related D252N mutation.Science China. Life sciences · 2023
   Article
7. Loss of TMEM106B exacerbates C9ALS/FTD DPR pathology by disrupting autophagosome maturation.Frontiers in cellular neuroscience · 2022
   Article
8. Lysosome dysfunction as a cause of neurodegenerative diseases: Lessons from frontotemporal dementia and amyotrophic lateral sclerosis.Neurobiology of disease · 2021
   Review
9. The Role of White Matter Dysfunction and Leukoencephalopathy/Leukodystrophy Genes in the Aetiology of Frontotemporal Dementias: Implications for Novel Approaches to Therapeutics.International journal of molecular sciences · 2021
   Review
10. Physiological and pathological functions of TMEM106B: a gene associated with brain aging and multiple brain disorders.Acta neuropathologica · 2021
    Review
11. Little Helpers or Mean Rogue-Role of Microglia in Animal Models of Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2021
    Review
12. Lysosomal Dysfunction and Other Pathomechanisms in FTLD: Evidence from Progranulin Genetics and Biology.Advances in experimental medicine and biology · 2021
    Article
13. Loss of TMEM106B potentiates lysosomal and FTLD-like pathology in progranulin-deficient mice.EMBO reports · 2020
    Article
14. Loss of Tmem106b exacerbates FTLD pathologies and causes motor deficits in progranulin-deficient mice.EMBO reports · 2020
    Article
15. A role of the frontotemporal lobar degeneration risk factor TMEM106B in myelination.Brain : a journal of neurology · 2020
    Article
16. Loss of TMEM106B leads to myelination deficits: implications for frontotemporal dementia treatment strategies.Brain : a journal of neurology · 2020
    Article
17. BV-2 Microglial Cells OverexpressingFrontiers in neurology · 2020
    Article
18. Astrocytes and Microglia as Potential Contributors to the Pathogenesis ofFrontiers in neuroscience · 2019
    Review
19. Lysosomal dysfunction inNeurology. Genetics · 2018
    Article

Corrections and comments

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Authors and funding

23 authors at 2 institutions in 1 country.

Funding

Abstract

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