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49/100

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Brain tissue and pathology

Topic: Brain proteins, microglia and lab models

Plain-language summary

Cytoplasmic aggregation of TAR DNA-binding protein 43 (TDP43; also known as TARDBP or TDP-43) is a key pathological feature of several neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). TDP43 typically resides in the nucleus but can shuttle between the nucleus and the cytoplasm to exert its multiple functions, which include regulation of the splicing, trafficking and stabilization of RNA. Cytoplasmic mislocalization and nuclear loss of TDP43 have both been associated with ALS and FTD, suggesting that calibrated levels and correct localization of TDP43 - achieved through an autoregulatory loop and tightly controlled nucleocytoplasmic transport - safeguard its normal function.

What this study adds

Evidence grade: Low

This is a narrative review. This review describes how TDP43 is normally controlled through autoregulation, localization and aggregation, and how mislocalization and nuclear loss are linked to ALS and FTD. It is a summary of biology, not a treatment or cure.

Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Tziortzouda, P., Van Den Bosch, L., & Hirth, F. (2021). Triad of TDP43 control in neurodegeneration: autoregulation, localization and aggregation. Nature reviews. Neuroscience. https://doi.org/10.1038/s41583-021-00431-1

Vancouver

Tziortzouda P, Van Den Bosch L, Hirth F. Triad of TDP43 control in neurodegeneration: autoregulation, localization and aggregation. Nature reviews. Neuroscience. 2021. doi:10.1038/s41583-021-00431-1. PMID: 33654312.

BibTeX

@article{tziortzouda2021-33654312,
  author  = {Tziortzouda, P. and Van Den Bosch, L. and Hirth, F.},
  title   = {{Triad of TDP43 control in neurodegeneration: autoregulation, localization and aggregation}},
  journal = {Nature reviews. Neuroscience},
  year    = {2021},
  doi     = {10.1038/s41583-021-00431-1},
  pmid    = {33654312},
  url     = {https://doi.org/10.1038/s41583-021-00431-1}
}

Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.

How to read this study

Design: this is a narrative review. It summarises a field without a fixed search method, so it shows how authors read the evidence rather than measuring it. Use it to find the primary studies, not as a result in itself.
Size: the record gives no participant count. Look for one in the original before trusting a pattern.
Effect: the record gives no effect size, so the summary above cannot say how large any difference was.

What the evidence grade means here

This page is graded low. alzhub.org assigns the grade automatically from keywords in the abstract, not from reading the paper. Low means the abstract matched neither pattern. It is the default label, and it does not mean the work is poor; many sound lab and imaging papers land here. It can add at most 5 of the 100 points in the study score, and it is a label about design, not a verdict on whether the findings are true.

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Key findings

TDP43 typically resides in the nucleus but can shuttle between the nucleus and the cytoplasm to exert its multiple functions, which include regulation of the splicing, trafficking and stabilization of RNA.
Cytoplasmic mislocalization and nuclear loss of TDP43 have both been associated with ALS and FTD, suggesting that calibrated levels and correct localization of TDP43 - achieved through an autoregulatory loop and tightly controlled nucleocytoplasmic transport - safeguard its normal function.
Furthermore, TDP43 can undergo phase transitions, including its dispersion into liquid droplets and its accumulation into irreversible cytoplasmic aggregates.
Thus, autoregulation, nucleocytoplasmic transport and phase transition are all part of an intrinsic control system regulating the physiological levels and localization of TDP43, and together are essential for the cellular homeostasis that is affected in neurodegenerative disease.

Why it matters

This review describes how TDP43 is normally controlled through autoregulation, localization and aggregation, and how mislocalization and nuclear loss are linked to ALS and FTD. It is a summary of biology, not a treatment or cure.

Study details

Evidence strengthLow

How this study scored 49/100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Nature reviews. Neuroscience)
Journal's citation record	4 / 4	Nature reviews. Neuroscience: journal h-index 572 (OpenAlex, 2026-10-29)
Study design	0 / 12	No study design recorded — scores zero, not guessed (not stated in the record — scored 0)
Strength of evidence	1 / 5	Rated “low” in our summary
Peer-review validation	10 / 10	Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent	3 / 5	2021 — within 6 year(s) of the newest study here
Sample size	0 / 4	Participant count not stated — scores zero (not stated in the record — scored 0)
Effect reported	0 / 3	No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people	0 / 3	Not stated whether this was studied in people — scores zero (not stated in the record — scored 0)
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	5 / 7	Cited 267 times (OpenAlex, 2026-10-10)
Citations per year	4 / 5	38.1 citations a year over 7 year(s) since 2021
Impact for its field and year	3 / 6	Cited 6.1× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	3 / 6	Cited by 12 other studies in this library
Still being cited	3 / 4	Cited 173 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	2 / 4	Last-listed author Frank Hirth: h-index 38 (OpenAlex, whole career)
Institution's track record	1 / 3	KU Leuven: institution h-index 1,386 (OpenAlex)
Multicenter collaboration	1 / 3	OpenAlex lists 3 institution(s) in 2 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 33654312)
Free to read	0 / 2	Behind a paywall — scores zero
Total	49 / 100	—

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