Evidence map›Paper›PMID 31039129›Full record

ArticleAging2019

Deletion of Tbk1 disrupts autophagy and reproduces behavioral and locomotor symptoms of FTD-ALS in mice.

Weisong Duan, Moran Guo, Le Yi, Jie Zhang, Yue Bi, Yakun Liu, Yuanyuan Li, Zhongyao Li, Yanqin Ma, Guisen Zhang and 3 more

Open access · greenAbstract read
In one paragraph

Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

33 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Role of the STING→IRF3 Pathway in Ambient GABA Homeostasis and Cognitive Function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Mitochondria-associated membrane collapse impairs TBK1-mediated proteostatic stress response in ALS.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  12. Article
  13. Functional Characterization of a Familial ALS-Associated MissenseInternational journal of molecular sciences · 2023
    Article
  14. Review
  15. Review
  16. Autophagy Dysfunction in ALS: from Transport to Protein Degradation.Journal of molecular neuroscience : MN · 2022
    Review
  17. The role of TBK1 in cancer pathogenesis and anticancer immunity.Journal of experimental & clinical cancer research : CR · 2022
    Review
  18. Modelling amyotrophic lateral sclerosis in rodents.Nature reviews. Neuroscience · 2022
    Review
  19. Article
  20. Review
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

13 authors at 3 institutions in 1 country.

Weisong DuanDepartment of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China.
Moran GuoDepartment of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China.
Le YiDepartment of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China.
Jie ZhangDepartment of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China.
Yue BiDepartment of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China.
Yakun LiuDepartment of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China.
Yuanyuan LiDepartment of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China.
Zhongyao LiDepartment of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China.
Yanqin MaJiangsu Nhwa Pharmaceutical Co. Ltd, Nantong 226000, People's Republic of China.
Guisen ZhangJiangsu Nhwa Pharmaceutical Co. Ltd, Nantong 226000, People's Republic of China.
Yaling LiuDepartment of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China.
Xueqing SongDepartment of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China.
Chunyan LiDepartment of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China.
Hebei Medical University · CNSecond Hospital of Hebei Medical University · CNJiangsu Nhwa Pharmaceutical (China) · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Haploinsufficiency of the protein kinase Tbk1 has shown to cause both amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD); however, the pathogenic mechanisms are unclear. Here we show that conditional neuronal deletion of Tbk1 in leads to cognitive and locomotor deficits in mice. Tbk1-NKO mice exhibited numerous neuropathological changes, including neurofibrillary tangles, abnormal dendrites, reduced dendritic spine density, and cortical synapse loss. The Purkinje cell layer of the cerebellum presented dendritic swelling, abnormally shaped astrocytes, and p62- and ubiquitin-positive aggregates, suggesting impaired autophagy. Inhibition of autophagic flux with bafilomycin A increased total Tkb1 levels in motor neuron-like cells

Indexed as

Amyotrophic Lateral SclerosisAnimalsAutophagyBehavior, AnimalCerebellumDisease Models, AnimalFrontotemporal DementiaMiceMice, KnockoutMotor ActivityMotor NeuronsPhosphorylationProtein Serine-Threonine KinasesProtein Serine-Threonine KinasesTbk1 protein, mouseamyotrophic lateral sclerosisautophagyfrontotemporal dementiap62Tbk1

Identifiers

PMID31039129
PMCPMC6519994
OpenAlexW2943626993

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.