2026-06-14T03:33:00Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/271522026-01-17T01:19:42Zcom_20.500.12105_2052com_20.500.12105_2051col_20.500.12105_19616

00925njm 22002777a 4500 dc Casas-Tinto, Sergio author Garcia-Guillen, Nuria author Losada-Perez, María author 2025-03-07 As the global population ages, the prevalence of neurodegenerative disorders is fast increasing. This neurodegeneration as well as other central nervous system (CNS) injuries cause permanent disabilities. Thus, generation of new neurons is the rosetta stone in contemporary neuroscience. Glial cells support CNS homeostasis through evolutionary conserved mechanisms. Upon damage, glial cells activate an immune and inflammatory response to clear the injury site from debris and proliferate to restore cell number. This glial regenerative response (GRR) is mediated by the neuropil-associated glia (NG) in , equivalent to vertebrate astrocytes, oligodendrocytes (OL), and oligodendrocyte progenitor cells (OPCs). Here, we examine the contribution of NG lineages and the GRR in response to injury. The results indicate that NG exchanges identities between ensheathing glia (EG) and astrocyte-like glia (ALG). Additionally, we found that NG cells undergo transdifferentiation to yield neurons. Moreover, this transdifferentiation increases in injury conditions. Thus, these data demonstrate that glial cells are able to generate new neurons through direct transdifferentiation. The present work makes a fundamental contribution to the CNS regeneration field and describes a new physiological mechanism to generate new neurons. Sergio Casas-Tinto, Nuria Garcia-Guillen, María Losada-Perez (2025) Adult neurogenesis through glial transdifferentiation in a CNS injury paradigm eLife 13:RP96890. https://doi.org/10.7554/eLife.96890.4. 10.7554/eLife.96890 Neuroscience 40052673 https://hdl.handle.net/20.500.12105/27152 CNS injury D. melanogaster Glia Neuroscience Regeneration Transdifferentiation Ventral nerve cord Adult neurogenesis through glial transdifferentiation in a CNS injury paradigm.