Loss of Cxcr5 alters neuroblast proliferation and migration in the aged brain

Jonas Fritze, Aurélie Ginisty, Rebecca McDonald, Ella Quist, Eleanor Stamp, Emanuela Monni, Parashar Dhapola, Stefan Lang, Henrik Ahlenius

Research output: Contribution to journalArticlepeer-review


Neurogenesis, the production of new neurons from neural stem cells, dramatically decreases during aging concomitantly with increased inflammation both systemically and in the brain. However, the precise role of inflammation and whether local or systemic factors drive the neurogenic decline during aging is poorly understood. Here, we identify CXCR5/5/CXCL13 signaling as a novel regulator of neurogenesis in the aged brain. The chemokine Cxcl13 was found to be upregulated in the brain during aging. Loss of its receptor, Cxcr5, led to increased proliferation and decreased numbers of neuroblasts in the aged subventricular zone (SVZ), together with accumulation of neuroblasts in the rostral migratory stream and olfactory bulb (OB), without increasing the amount of new mature neurons in the OB. The effect on proliferation and migration was specific to neuroblasts and likely mediated through increased levels of systemic IL-6 and local Cxcl12 expression in the SVZ. Our study raises the possibility of a new mechanism by which interplay between systemic and local alterations in inflammation regulates neurogenesis during aging.

Original languageEnglish
Pages (from-to)1175-1187
JournalStem Cells
Issue number9
Early online date2020
Publication statusPublished - 2020

Subject classification (UKÄ)

  • Neurosciences

Free keywords

  • aging
  • Cxcl13
  • Cxcr5
  • neuroblast
  • neurogenesis


Dive into the research topics of 'Loss of Cxcr5 alters neuroblast proliferation and migration in the aged brain'. Together they form a unique fingerprint.

Cite this