Home › Research › Disease mechanisms
KCTD20 Suppression as a Potential Therapeutic Strategy against Neurodegenerative Tauopathies
Dinesh Kumar, Vrinda Gupta, Nicky Kumar Jaiswal, Rajni Tanwar, Pooja Rani. Current Neuroscience, 2026-04-07
Topic: Brain proteins, microglia and lab models
Abstract: The accumulation of tau proteins in the brain contributes to the therapeutic challenges faced by patients with Alzheimer’s disease, frontotemporal dementia, and other neurodegenerative disorders. It has been found that KCTD20 suppression is a crucial therapeutic target for preventing tau protein degeneration triggered by glutamate. KCTD20 knockdown with either siRNA or antisense oligonucleotide increases lysosomal exocytosis and suppresses tau aggregation, as well as increases the survival of neurons. To illustrate this new preclinical modality, scientists combined patient- derived organoids with animal models, a strategy that may revolutionize future clinical therapies for neurodegenerative diseases.
Key findings
- Abstract: The accumulation of tau proteins in the brain contributes to the therapeutic challenges faced by patients with Alzheimer’s disease, frontotemporal dementia, and other neurodegenerative disorders.
- It has been found that KCTD20 suppression is a crucial therapeutic target for preventing tau protein degeneration triggered by glutamate.
- KCTD20 knockdown with either siRNA or antisense oligonucleotide increases lysosomal exocytosis and suppresses tau aggregation, as well as increases the survival of neurons.
- To illustrate this new preclinical modality, scientists combined patient- derived organoids with animal models, a strategy that may revolutionize future clinical therapies for neurodegenerative diseases.
Why it matters
In preclinical work using patient-derived organoids and animal models, suppressing KCTD20 with siRNA or antisense oligonucleotide increased lysosomal exocytosis, reduced tau aggregation and increased neuron survival. This is early laboratory research, and the authors describe it as a new preclinical modality rather than a proven treatment.
Study details
- Evidence strengthLow
How this study scored 25/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Current Neuroscience) |
| Journal's citation record | 0 / 4 | Current Neuroscience: journal h-index 0 (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 | 5 / 5 | 2026 — within 1 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) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 0 / 7 | Cited 0 times (OpenAlex, 2026-10-10) |
| Citations per year | 0 / 5 | 0.0 citations a year over 2 year(s) since 2026 |
| Impact for its field and year | 0 / 6 | Cited 0.0× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 0 / 4 | Cited 0 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 0 / 4 | Last-listed author Pooja Rani: h-index 4 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | Guru Jambheshwar University of Science and Technology: institution h-index 200 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 1 country |
| Indexed in PubMed | 1 / 2 | Not in PubMed, but has a DOI |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 25 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
May need a subscription OpenAlex found no free copy of the full text (checked 6 Feb 1020), so the publisher may charge for it.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
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.
APA 7th
Kumar, D., Gupta, V., Jaiswal, N. K., Tanwar, R., & Rani, P. (2026). KCTD20 Suppression as a Potential Therapeutic Strategy against Neurodegenerative Tauopathies. Current Neuroscience. https://doi.org/10.2174/0129505623425326251026172237
Vancouver
Kumar D, Gupta V, Jaiswal NK, Tanwar R, Rani P. KCTD20 Suppression as a Potential Therapeutic Strategy against Neurodegenerative Tauopathies. Current Neuroscience. 2026. doi:10.2174/0129505623425326251026172237.
BibTeX
@article{kumar2026-a34e3884,
author = {Kumar, Dinesh and Gupta, Vrinda and Jaiswal, Nicky Kumar and Tanwar, Rajni and Rani, Pooja},
title = {{KCTD20 Suppression as a Potential Therapeutic Strategy against Neurodegenerative Tauopathies}},
journal = {Current Neuroscience},
year = {2026},
doi = {10.2174/0129505623425326251026172237},
url = {https://doi.org/10.2174/0129505623425326251026172237}
}
Related studies in Disease mechanisms
Also tagged “phosphorylated”
732 studies in the library carry the topic tag “phosphorylated”; these are this study's neighbours in a fixed, alphabetical-by-hash tour of them, not the closest in content. All 732 tagged studies.