Evidence map›Paper›PMID 27725660›Full record

ReviewMolecular psychiatry2017

Interrogating the mouse thalamus to correct human neurodevelopmental disorders.

L I Schmitt, M M Halassa

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
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  4. Article
  5. When the central integrator disintegrates: A review of the role of the thalamus in cognition and dementia.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Review
  6. Review
  7. Increased resting-state thalamocortical functional connectivity in children and young adults with autism spectrum disorder.Autism research : official journal of the International Society for Autism Research · 2023
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
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.

L I SchmittThe Neuroscience Institute, New York University School of Medicine, New York, NY, USA.
M M HalassaThe Neuroscience Institute, New York University School of Medicine, New York, NY, USA.
New York University · USNYU Langone Health · US

Funding

Dissecting the role of thalamic inhibition in neurodevelopmental diseasesR01NS098505 · NINDS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI FENG, GUOPING, HALASSA, MICHAEL M · 2016 to 2020
$3.2M
The cognitive searchlight: TRN circuit dissection in health and diseaseR01MH107680 · NIMH · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI HALASSA, MICHAEL M · 2015 to 2019
$2.5M
Causal examination of TRN role in neocortical spindle generation and functionR00NS078115 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI HALASSA, MICHAEL M · 2014 to 2016
$747k
NIMH NIH HHS R01 MH107680NINDS NIH HHS R00 NS078115NINDS NIH HHS R01 NS098505
6 · The paper itself

Abstract

While localizing sensory and motor deficits is one of the cornerstones of clinical neurology, behavioral and cognitive deficits in psychiatry remain impervious to this approach. In psychiatry, major challenges include the relative subtlety by which neural circuits are perturbed, and the limited understanding of how basic circuit functions relate to thought and behavior. Neurodevelopmental disorders offer a window to addressing the first challenge given their strong genetic underpinnings, which can be linked to biological mechanisms. Such links have benefited from genetic modeling in the mouse, and in this review we highlight how this small mammal is now allowing us to crack neural circuits as well. We review recent studies of mouse thalamus, discussing how they revealed general principles that may underlie human perception and attention. Controlling the magnitude (gain) of thalamic sensory responses is a mechanism of attention, and the mouse has enabled its functional dissection at an unprecedented resolution. Further, modeling human genetic neurodevelopmental disease in the mouse has shown how diminished thalamic gain control can lead to attention deficits. This breaks new ground in how we untangle the complexity of psychiatric diseases; by making thalamic circuits accessible to mechanistic dissection; the mouse has not only taught us how they fundamentally work, but also how their dysfunction can be precisely mapped onto behavioral and cognitive deficits. Future studies promise even more progress, with the hope that principled targeting of identified thalamic circuits can be uniquely therapeutic.

Indexed as

AnimalsAttentionBehavior, AnimalHumansMiceModels, AnimalNeural PathwaysNeurodevelopmental DisordersThalamus

Identifiers

PMID27725660
PMCPMC5258688
OpenAlexW2531751353

What OpenQuestion holds

Textmetadata
LicenceTDM
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.