Evidence map›Paper›PMID 38238329›Full record

ArticleNature communications2024

Acetylcholine receptor based chemogenetics engineered for neuronal inhibition and seizure control assessed in mice.

Quynh-Anh Nguyen, Peter M Klein, Cheng Xie, Katelyn N Benthall, Jillian Iafrati, Jesslyn Homidan, Jacob T Bendor, Barna Dudok, Jordan S Farrell, Tilo Gschwind and 4 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 3 institutions in 1 country.

Quynh-Anh Nguyen *Department of Neurosurgery, Stanford University, Stanford, CA, 94305, USA. qanguyen@stanford.edu.ORCID 0000-0003-4910-7899
Peter M Klein *Department of Neurosurgery, Stanford University, Stanford, CA, 94305, USA. kleinp@stanford.edu.ORCID 0000-0002-3232-3387
Cheng XieCODA Biotherapeutics, 240 East Grand Ave., South San Francisco, CA, 94080, USA.
Katelyn N BenthallCODA Biotherapeutics, 240 East Grand Ave., South San Francisco, CA, 94080, USA.
Jillian IafratiCODA Biotherapeutics, 240 East Grand Ave., South San Francisco, CA, 94080, USA.
Jesslyn HomidanDepartment of Neurosurgery, Stanford University, Stanford, CA, 94305, USA.
Jacob T BendorCODA Biotherapeutics, 240 East Grand Ave., South San Francisco, CA, 94080, USA.
Barna DudokDepartment of Neurosurgery, Stanford University, Stanford, CA, 94305, USA.ORCID 0000-0001-5078-0090
Jordan S FarrellDepartment of Neurosurgery, Stanford University, Stanford, CA, 94305, USA.ORCID 0000-0002-1209-5559
Tilo GschwindDepartment of Neurosurgery, Stanford University, Stanford, CA, 94305, USA.
Charlotte L PorterDepartment of Neurosurgery, Stanford University, Stanford, CA, 94305, USA.ORCID 0009-0009-9750-9148
Annahita KeravalaCODA Biotherapeutics, 240 East Grand Ave., South San Francisco, CA, 94080, USA.
G Steven DodsonCODA Biotherapeutics, 240 East Grand Ave., South San Francisco, CA, 94080, USA.
Ivan SolteszDepartment of Neurosurgery, Stanford University, Stanford, CA, 94305, USA.ORCID 0000-0003-1493-3744
Stanford University · USStanford Medicine · USBaylor College of Medicine · US

Funding

VECTOR COREP30NS069375 · NINDS · STANFORD UNIVERSITY · PI SHAMLOO, MEHRDAD · 2011 to 2019
$6.3M
NINDS NIH HHS P30 NS069375
6 · The paper itself

Abstract

Epilepsy is a prevalent disorder involving neuronal network hyperexcitability, yet existing therapeutic strategies often fail to provide optimal patient outcomes. Chemogenetic approaches, where exogenous receptors are expressed in defined brain areas and specifically activated by selective agonists, are appealing methods to constrain overactive neuronal activity. We developed BARNI (Bradanicline- and Acetylcholine-activated Receptor for Neuronal Inhibition), an engineered channel comprised of the α7 nicotinic acetylcholine receptor ligand-binding domain coupled to an α1 glycine receptor anion pore domain. Here we demonstrate that BARNI activation by the clinical stage α7 nicotinic acetylcholine receptor-selective agonist bradanicline effectively suppressed targeted neuronal activity, and controlled both acute and chronic seizures in male mice. Our results provide evidence for the use of an inhibitory acetylcholine-based engineered channel activatable by both exogenous and endogenous agonists as a potential therapeutic approach to treating epilepsy.

Indexed as

EpilepsyReceptors, NicotinicAcetylcholinealpha7 Nicotinic Acetylcholine ReceptorAnimalsHumansMaleMiceNicotinic AgonistsReceptors, CholinergicSeizuresAcetylcholinealpha7 Nicotinic Acetylcholine ReceptorNicotinic AgonistsReceptors, CholinergicReceptors, Nicotinic

Identifiers

PMID38238329
PMCPMC10796428
OpenAlexW4390964665

What OpenQuestion holds

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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.