Evidence map›Paper›PMID 27375444›Full record

ReviewFrontiers in behavioral neuroscience2016

DYRK1A, a Dosage-Sensitive Gene Involved in Neurodevelopmental Disorders, Is a Target for Drug Development in Down Syndrome.

Arnaud Duchon, Yann Herault

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in behavioral neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed
15.4field-weighted citation impact, top 1% 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

115 citing papers in PubMed, 180 citations in OpenAlex.

  1. Article
  2. Sex-specific developmental phenotypes and their response to neonatalbioRxiv : the preprint server for biology · 2026
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  17. Plasma p-tau212 as a biomarker of sporadic and Down syndrome Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  18. Review
  19. Article
  20. Article

55 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

Arnaud DuchonDepartment of Translational Medicine and Neurogenetics, Institut de Génétique et de Biologie Moléculaire et CellulaireIllkirch, France; UMR7104, Centre National de la Recherche ScientifiqueIllkirch, France; U964, Institut National de la Santé et de la Recherche MédicaleIllkirch, France; Université de StrasbourgIllkirch, France.
Yann HeraultDepartment of Translational Medicine and Neurogenetics, Institut de Génétique et de Biologie Moléculaire et CellulaireIllkirch, France; UMR7104, Centre National de la Recherche ScientifiqueIllkirch, France; U964, Institut National de la Santé et de la Recherche MédicaleIllkirch, France; Université de StrasbourgIllkirch, France; PHENOMIN, Institut Clinique de la Souris, Groupement d'Intérêt Économique-Centre Européen de Recherche en Biologie et en Médecine, CNRS, INSERMIllkirch-Graffenstaden, France.
Institut de génétique et de biologie moléculaire et cellulaire · FRUniversité de Strasbourg · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Down syndrome (DS) is one of the leading causes of intellectual disability, and patients with DS face various health issues, including learning and memory deficits, congenital heart disease, Alzheimer's disease (AD), leukemia, and cancer, leading to huge medical and social costs. Remarkable advances on DS research have been made in improving cognitive function in mouse models for future therapeutic approaches in patients. Among the different approaches, DYRK1A inhibitors have emerged as promising therapeutics to reduce DS cognitive deficits. DYRK1A is a dual-specificity kinase that is overexpressed in DS and plays a key role in neurogenesis, outgrowth of axons and dendrites, neuronal trafficking and aging. Its pivotal role in the DS phenotype makes it a prime target for the development of therapeutics. Recently, disruption of DYRK1A has been found in Autosomal Dominant Mental Retardation 7 (MRD7), resulting in severe mental deficiency. Recent advances in the development of kinase inhibitors are expected, in the near future, to remove DS from the list of incurable diseases, providing certain conditions such as drug dosage and correct timing for the optimum long-term treatment. In addition the exact molecular and cellular mechanisms that are targeted by the inhibition of DYRK1A are still to be discovered.

Indexed as

clinical trialcognitionDYRK1A and kinase inhibitorslearning and memorymouse modelneurodevelopmental disordertrisomy 21

Identifiers

PMID27375444
PMCPMC4891327
OpenAlexW2468259612

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.