Alyssa Puno
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Alyssa Puno has a total of 13 co-authors. Here are the top co-authors by number of shared publications:
Amanda Everitt
Department of Psychiatry and Behavioral Sciences, UCSF Weill Institute for Neurosciences, University of California, San Francisco
1 shared publication- Anca M. Pasca
Stanford University
1 shared publication Dhriti Nagar
Department of Pediatrics, Stanford University
1 shared publicationEmily Gurwitz
Department of Pediatrics, Stanford University
1 shared publicationFikri Birey
Department of Human Genetics, Emory University
1 shared publicationJeremy A Willsey
Department of Psychiatry and Behavioral Sciences, UCSF Weill Institute for Neurosciences, University of California, San Francisco
1 shared publication
Latest Publications
- Open Access
- 15 May 2026
- Published by eLife Sciences Publications, Ltd in eLife
- Vol. 14
Adrenomedullin restores the human cortical interneurons migration defects induced by hypoxia
Extremely preterm birth (at ADM ) as the gene with the highest fold change increase in expression. Based on previous literature about the protective role of supplemental ADM for other injuries, here, we demonstrated that addition of exogenous ADM to the hypoxic media restores the migration defects of interneurons. Lastly, we showed that one of the mechanisms of protection by ADM is through the activation of the cAMP/PKA pathway and subsequent pCREB-dependent rescued expression of a subset of GABA receptors, which are known to promote migration. Overall, in this manuscript, we provide the first direct evidence for hypoxia-induced deficits in the migration of human cortical interneurons and identify ADM as a possible target for therapeutic development.
- 15 May 2026
- Published by eLife Sciences Publications, Ltd in eLife
- Vol. 14
Open AccessAdrenomedullin restores the human cortical interneurons migration defects induced by hypoxia
Extremely preterm birth (at ADM ) as the gene with the highest fold change increase in expression. Based on previous literature about the protective role of supplemental ADM for other injuries, here, we demonstrated that addition of exogenous ADM to the hypoxic media restores the migration defects of interneurons. Lastly, we showed that one of the mechanisms of protection by ADM is through the activation of the cAMP/PKA pathway and subsequent pCREB-dependent rescued expression of a subset of GABA receptors, which are known to promote migration. Overall, in this manuscript, we provide the first direct evidence for hypoxia-induced deficits in the migration of human cortical interneurons and identify ADM as a possible target for therapeutic development.