PuSH - Publikationsserver des Helmholtz Zentrums München

Ware, K.* ; Peter, J.* ; Yazell, J.* ; Thapa, C.* ; Taranov, A.* ; Bedolla, A.* ; Distel, C.* ; Lammich, S.* ; Feederle, R. ; Sülzen, A.* ; Liddelow, S.* ; Roskin, K.* ; Luo, Y.*

Inhibition of TGF-β signaling in microglia stimulates hippocampal adult neurogenesis and reduces anxiety-like behavior in adult mice.

Nat. Commun. 17:1440 (2026)
Verlagsversion Forschungsdaten DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Adult neurogenesis in the subgranular zone (SGZ) has been implicated in cognitive and affective functions. The role of neuroinflammation and reactive microglia in SGZ neurogenesis is not well understood. TGF-β signaling is critical to maintaining microglia homeostasis in the adult brain. To investigate the role of microglia in SGZ neurogenesis, using microglia-specific inducible knockout (iKO) mice for TGF-β1 ligand or receptor (Alk5 or Tgfbr2), here we show that TGF-β-deficient microglia increase adult neurogenesis in the SGZ, accompanied by altered anxiety-like behavior in KO mice. Single-cell RNAseq (ScRNAseq) analysis shows decreased PTEN signaling, and immunohistochemistry shows increased mTOR activity in DCX+ newly born neuroblasts at the SGZ in iKO mice. Inhibition of mTOR signaling by rapamycin reverses the heightened SGZ neurogenesis in iKO mice. This study reveals the role of microglia in regulating hippocampal adult neurogenesis via the PTEN-mTOR pathway and its potential implications for behavioral and affective functions.
Altmetric
Weitere Metriken?
[➜Einloggen]
Zusatzinfos bearbeiten [➜Einloggen]
Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Neurogenesis ; Microglia ; Hippocampal Formation ; Hippocampus ; Central Nervous System ; Signal Transduction; Dentate Gyrus; Stem-cells; Receptor; Brain; Roles; Mouse; Oligodendrogenesis; Sufficient; Pathway; Target
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Zeitschrift Nature Communications
Quellenangaben Band: 17, Heft: 1, Seiten: , Artikelnummer: 1440 Supplement: ,
Verlag Springer
Verlagsort London
Begutachtungsstatus Peer reviewed
Institut(e) CF Monoclonal Antibodies (CF-MAB)
Förderungen University of Cincinnati (UC)
U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke (NINDS)