Evidence map›Paper›PMID 42138713›Full record

ArticleeLife2026

Adrenomedullin restores the human cortical interneurons migration defects induced by hypoxia.

Alyssa Puno, Wojciech P Michno, Li Li, Amanda Everitt, Kate McCluskey, Saw Htun, Dhriti Nagar, Jong Bin Choi, Yuqin Dai, Seyeon Park and 4 more

Abstract read
In one paragraph

Article in eLife, 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
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

14 authors.

Alyssa Puno *Department of Pediatrics, Stanford University, Stanford, United States.ORCID https://orcid.org/0009-0001-8342-5324
Wojciech P Michno *Department of Pediatrics, Stanford University, Stanford, United States.ORCID https://orcid.org/0000-0002-3096-3604
Li LiDepartment of Pediatrics, Stanford University, Stanford, United States.
Amanda EverittDepartment of Psychiatry and Behavioral Sciences, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, United States.
Kate McCluskeyDepartment of Psychiatry and Behavioral Sciences, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, United States.
Saw HtunDepartment of Pediatrics, Stanford University, Stanford, United States.
Dhriti NagarDepartment of Pediatrics, Stanford University, Stanford, United States.
Jong Bin ChoiDepartment of Pediatrics, Stanford University, Stanford, United States.ORCID https://orcid.org/0000-0002-7017-1775
Yuqin DaiSarafan ChEM-H, Stanford University, Stanford, United States.
Seyeon ParkDepartment of Pediatrics, Stanford University, Stanford, United States.
Emily GurwitzDepartment of Pediatrics, Stanford University, Stanford, United States.
Jeremy A WillseyDepartment of Psychiatry and Behavioral Sciences, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, United States.
Fikri BireyDepartment of Human Genetics, Emory University, Atlanta, United States.
Anca M PascaDepartment of Pediatrics, Stanford University, Stanford, United States.ORCID https://orcid.org/0000-0002-0445-9009

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Extremely preterm birth (at <28 postconceptional weeks) leads to brain injury and represents the leading cause of childhood-onset neuropsychiatric diseases. No effective therapeutics exist to reduce the incidence and severity of brain injury of prematurity. Hypoxic events are the most important environmental factor, along with inflammation. Among other developmental processes, the second half of in utero fetal development coincides with the migration of cortical interneurons from the ganglionic eminences into the cortex; this process is thus prone to disruptions following extremely preterm birth. To date, no studies have directly investigated the migration of human cortical inhibitory neurons under hypoxic conditions. Using multi-day confocal live imaging in human forebrain assembloids (hFA) derived from human-induced pluripotent stem cells (hiPSCs) and ex vivo developing human brain tissue, we found a substantial reduction in the migration of hypoxic interneurons. Using transcriptomics, we identified adrenomedullin (

Indexed as

AdrenomedullinCell MovementCerebral CortexHypoxiaInterneuronsCell HypoxiaHumansInduced Pluripotent Stem CellsNeurodevelopmentAdrenomedullinadrenomedullinassembloidshumanhypoxiainterneuronsneonatalneuroscienceregenerative medicinestem cells

Identifiers

PMID42138713
PMCPMC13179061

What Socratic 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 Socratic graph.