Evidence map›Paper›PMID 31078519›Full record

ReviewEBioMedicine2019

Designer receptor technology for the treatment of epilepsy.

Andreas Lieb, Mikail Weston, Dimitri M Kullmann

Open access · goldAbstract readReview
In one paragraph

Review in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 46 citations in OpenAlex.

  1. Overview of the DREADDs chemogenetics and the patent landscape of their actuators.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026
    Review
  2. Article
  3. Article
  4. Chemogenetics with PSAMGene therapy · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Reactivation of Early-Life Stress-Sensitive Neuronal Ensembles Contributes to Lifelong Stress Hypersensitivity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Chronic Behavioral Manipulation via Orally Delivered Chemogenetic Actuator in Macaques.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  14. Review
  15. Gene and Cell Therapy for Epilepsy: A Mini Review.Frontiers in molecular neuroscience · 2022
    Review
  16. Review
  17. DREADDs in Epilepsy Research: Network-Based Review.Frontiers in molecular neuroscience · 2022
    Review
  18. Review
  19. European journal of medicinal chemistry · 2021
    Article
  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

3 authors at 2 institutions in 1 country.

Andreas LiebDepartment of Clinical and Experimental Epilepsy, UCL Queen Square Institute of Neurology, University College London, UK.
Mikail WestonDepartment of Clinical and Experimental Epilepsy, UCL Queen Square Institute of Neurology, University College London, UK.
Dimitri M KullmannDepartment of Clinical and Experimental Epilepsy, UCL Queen Square Institute of Neurology, University College London, UK. Electronic address: d.kullmann@ucl.ac.uk.
National Hospital for Neurology and Neurosurgery · GBUniversity College London · GB

Funding

Medical Research Council G0802158Medical Research Council G116/147Medical Research Council MR/L01095X/1Wellcome Trust 209807/Z/17/ZWellcome Trust 212285/Z/18/Z
6 · The paper itself

Abstract

Epilepsy remains refractory to medical treatment in ~30% of patients despite decades of new drug development. Neurosurgery to remove or disconnect the seizure focus is often curative but frequently contraindicated by risks of irreversible impairment to brain function. Novel therapies are therefore required that better balance seizure suppression against the risks of side effects. Among experimental gene therapies, chemogenetics has the major advantage that the action on the epileptogenic zone can be modulated on demand. Two broad approaches are to use a designer G-protein-coupled receptor or a modified ligand gated ion channel, targeted to specific neurons in the epileptogenic zone using viral vectors and cell-type selective promoters. The receptor can be activated on demand by either an exogenous compound or by pathological levels of extracellular glutamate that occur in epileptogenic tissue. We review the principal designer receptor technologies and their modes of action. We compare the drawbacks and benefits of each designer receptor with particular focus on the drug activators and the potential for clinical translation in epilepsy.

Indexed as

Drug DesignAnimalsEpilepsyHumansIon Channel GatingLigandsMolecular Targeted TherapyQuantitative Structure-Activity RelationshipReceptors, G-Protein-CoupledLigandsReceptors, G-Protein-CoupledChemogeneticsDesigner receptorDREADDGluClhM4D(Gi)PSAM

Identifiers

PMID31078519
PMCPMC6558262
OpenAlexW2944011421

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.