RT Journal Article
T1 Post-stroke Neurogenesis: Friend or Foe?
A1 Cuartero Desviat, María Isabel
A1 García Culebras, Alicia
A1 Torres López, Cristina
A1 Medina, Violeta
A1 Fraga, Enrique
A1 Vázquez-Reyes, Sandra
A1 Jareño-Flores, Tania
A1 García Segura, Juan Manuel
A1 Lizasoaín Hernández, Ignacio
A1 Moro Sánchez, María Ángeles
AB The substantial clinical burden and disability after stroke injury urges the need to explore therapeutic solutions. Recent compelling evidence supports that neurogenesis persists in the adult mammalian brain and is amenable to regulation in both physiological and pathological situations. Its ability to generate new neurons implies a potential to contribute to recovery after brain injury. However, post-stroke neurogenic response may have different functional consequences. On the one hand, the capacity of newborn neurons to replenish the damaged tissue may be limited. In addition, aberrant forms of neurogenesis have been identified in several insult settings. All these data suggest that adult neurogenesis is at a crossroads between the physiological and the pathological regulation of the neurological function in the injured central nervous system (CNS). Given the complexity of the CNS together with its interaction with the periphery, we ultimately lack in-depth understanding of the key cell types, cell–cell interactions, and molecular pathways involved in the neurogenic response after brain damage and their positive or otherwise deleterious impact. Here we will review the evidence on the stroke-induced neurogenic response and on its potential repercussions on functional outcome. First, we will briefly describe subventricular zone (SVZ) neurogenesis after stroke beside the main evidence supporting its positive role on functional restoration after stroke. Then, we will focus on hippocampal subgranular zone (SGZ) neurogenesis due to the relevance of hippocampus in cognitive functions; we will outline compelling evidence that supports that, after stroke, SGZ neurogenesis may adopt a maladaptive plasticity response further contributing to the development of post-stroke cognitive impairment and dementia. Finally, we will discuss the therapeutic potential of specific steps in the neurogenic cascade that might ameliorate brain malfunctioning and the development of post-stroke cognitive impairment in the chronic phase.</jats:p>
PB Frontiers
SN 2296-634X
YR 2021
FD 2021
LK https://hdl.handle.net/20.500.14352/94629
UL https://hdl.handle.net/20.500.14352/94629
LA eng
NO Cuartero MI, García-Culebras A, Torres-López C, Medina V, Fraga E, Vázquez-Reyes S, Jareño-Flores T, García-Segura JM, Lizasoain I and Moro MÁ (2021) Post-stroke Neurogenesis: Friend or Foe? Front. Cell Dev. Biol. 9:657846. doi: 10.3389/fcell.2021.657846
NO This work was supported by the grants from Spanish Ministry of Science and Innovation, PID2019-106581RB-I00 (MM); Leducq Foundation for Cardiovascular Research, TNE-19CVD01 (MM); Fundación La Caixa, HR17_00527 (MM); Instituto de Salud Carlos III and co-financed by the European Development Regional Fund “A Way to Achieve Europe,” PI20/00535 and RETICS RD16/0019/0009 (IL); by contracts FJC-039343-I (AG-C) from the Spanish Ministry of Science and Innovation; and FPU01405265 (VM) and FPU19/02989 (EF) from the Spanish Ministry of Universities. The CNIC is supported by the Instituto de Salud Carlos III (ISCIII), the Ministerio de Ciencia e Innovación (MCIN), and the Pro CNIC Foundation and is a Severo Ochoa Center of Excellence (SEV-2015-0505).
NO Leducq Foundation for Cardiovascular Research
NO Fundación La Caixa
NO Instituto de Salud Carlos III
NO European Commission
NO Ministerio de Ciencia, Innovación y Universidades (España)
DS Docta Complutense
RD 10 abr 2025