In one paragraphArticle in Science advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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 registryThe 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 literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
23 authors.
Travis E FaustDepartment of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.ORCID 0000-0002-4567-8435 Atsushi SaitoDepartment of Physiology, Pharmacology, and Therapeutics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.ORCID 0000-0001-5304-5286 Shoichi IshikawaDepartment of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Kun YangDepartment of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.ORCID 0000-0002-1060-8082 Wendy XinDepartment of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.ORCID 0000-0002-1425-834X Ho NamkungDepartment of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.ORCID 0000-0003-0744-1020 Amit AgarwalDepartment of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.ORCID 0000-0001-7948-4498 Adriana RamosDepartment of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.ORCID 0009-0002-4337-1533 Brian J LeeDepartment of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Lindsay HayesDepartment of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.ORCID 0000-0001-6314-6451 Rupali SrivastavaDepartment of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Sunday AdelakunDepartment of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.ORCID 0000-0002-8328-3119 Sneha SahaDepartment of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Trexy PalenDepartment of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.ORCID 0000-0002-2374-9474 Tyler Cash-PadgettDepartment of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.ORCID 0000-0001-8977-3971 Daniel J WoodDepartment of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.ORCID 0000-0003-1874-7738 Elisa CarloniDepartment of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Ryosuke YusaDepartment of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Hanna Jaaro-PeledDepartment of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.ORCID 0000-0002-8950-391X Jed W FaheyDepartment of Physiology, Pharmacology, and Therapeutics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.ORCID 0000-0002-2129-1834 Dwight E BerglesDepartment of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.ORCID 0000-0002-7133-7378 Koko IshizukaDepartment of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Akira SawaDepartment of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.ORCID 0000-0003-1401-3008 Funding
Project 3P50MH094268 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SAWA, AKIRA · 2011 to 2020
$19.9MProject 3P50MH136297 · NIMH · JOHNS HOPKINS UNIVERSITY · PI Akira Sawa · 2024 to 2026
$12.8MMurine Mutagenesis CoreP30NS050274 · NINDS · JOHNS HOPKINS UNIVERSITY · PI KOLODKIN, ALEX L · 2005 to 2020
$10.9MHigh throughput marker for cognitive deficit: cellular autofluorescenceR01MH107730 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SAWA, AKIRA · 2018 to 2022
$3.0MDISC1-dependent defects in neural fate, corticogenesis and cognition in psychosisR01MH105660 · NIMH · JOHNS HOPKINS UNIVERSITY · PI ISHIZUKA, KOKO, SAWA, AKIRA · 2014 to 2018
$2.8MNIMH NIH HHS P50 MH094268NIMH NIH HHS P50 MH136297NIMH NIH HHS R01 MH105660NIMH NIH HHS R01 MH107730NINDS NIH HHS P30 NS050274
6 · The paper itselfAbstract
A fundamental but unanswered question in neuropsychiatry is whether the psychiatric symptoms of epilepsy are caused by the same or a separate pathophysiology as seizures. To address this question, we investigated a monogenic form of epilepsy (pyridoxine-dependent epilepsy) caused by aldehyde dehydrogenase 7 family member A1 (ALDH7A1) mutations. ALDH7A1 global knockout mice exhibited both seizure-associated and maladaptive affective behavioral phenotypes. However, seizure phenotypes were caused by ALDH7A1 deletion in hepatocytes whereas maladaptive affective behaviors were caused by ALDH7A1 deletion in astrocytes. Deletion in astrocytes disrupted astrocyte redox homeostasis, impairing regulation of extracellular ion concentrations and reducing neuronal activity in the prelimbic cortex. Sulforaphane, which activates the NRF2 antioxidant pathway, restored prelimbic neuronal activity and rescued maladaptive affective behaviors in ALDH7A1 knockout mice but did not prevent seizures. These studies implicate astrocyte redox homeostasis and prelimbic hypoactivity in maladaptive affective behavioral phenotypes in a congenital form of epilepsy, which are mechanistically and therapeutically dissociable from seizure pathophysiology.
Indexed as
AstrocytesEpilepsyNeuronsAldehyde DehydrogenaseAnimalsBehavior, AnimalDisease Models, AnimalIsothiocyanatesMaleMiceMice, KnockoutNF-E2-Related Factor 2Oxidation-ReductionSeizuresSulfoxidesAldehyde DehydrogenaseIsothiocyanatesNF-E2-Related Factor 2sulforaphaneSulfoxides
Identifiers
PMID42525741
PMCPMC13418531
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