ArticleExperimental biology and medicine (Maywood, N.J.)2020
Cytoplasmic mislocalization and mitochondrial colocalization of TDP-43 are common features between normal aged and young mice.
Article in Experimental biology and medicine (Maywood, N.J.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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
7 citing papers in PubMed.
- Stress granules as a central hub linking organelle stress, aging, and neurodegeneration.BMB reports · 2026Review
- Cell Stress Induces Mislocalization of Transcription Factors with Mitochondrial Enrichment.International journal of molecular sciences · 2021Article
- Mitochondrion-Dependent Cell Death in TDP-43 Proteinopathies.Biomedicines · 2021Review
- hnRNP A1B, a Splice Variant ofFrontiers in neuroscience · 2021Article
- Cytosolic calcium regulates cytoplasmic accumulation of TDP-43 through Calpain-A and Importin α3.eLife · 2020Article
- Mechanisms of aging, age-associated diseases, and lifespan determination.Experimental biology and medicine (Maywood, N.J.) · 2020Article
- Maintaining the balance of TDP-43, mitochondria, and autophagy: a promising therapeutic strategy for neurodegenerative diseases.Translational neurodegeneration · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
impact statementDespite increasing evidence implicating the important role of TDP-43 in the pathogenesis of a wide range of age-related neurodegenerative diseases, there is limited study of TDP-43 proteinopathy and its association with mitochondria during normal aging. Our findings of cytoplasmic accumulation of TDP-43 that is highly colocalized with mitochondria in neurons in selective brain regions in young animals in the absence of neuronal loss provide a novel insight into the development of TDP-43 proteinopathy and its contribution to neuronal loss.
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Registered trials
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.