bims-adhine Biomed News
on Adult hippocampal neurogenesis
Issue of 2026–08–09
two papers selected by
Tamara J. Buijs, Universiteit van Amsterdam
  1. Sox5 controls cell cycle progression in intermediate progenitor cells during dentate gyrus development.
  2. Chronic Smoking Impairs Glymphatic Transport and Cognitive Function in Adolescent Mice Through Cardiac, Vascular, and Perivascular Aquaporin-4 Mechanisms.
  1. Front Cell Dev Biol. 2026 ;14 1876208
    Sox5 controls cell cycle progression in intermediate progenitor cells during dentate gyrus development.
    Paula Tirado-Melendro, Lingling Li, Cristina Medina-Menéndez, Pilar Jurado-Angulo, Pilar Rodríguez-Martín, Laura García-Redondo, Katarzyna Bilińska, Aixa V Morales.
      The development of the dentate gyrus (DG) of the hippocampus is protracted over time in comparison with other brain regions such as hippocampal cornus ammoni or neocortex, extending over the first postnatal weeks. During DG postnatal development, neural stem cells (NSCs) will remain to generate the adult neurogenic niche that will sustain granule neuron (GN) production throughout life. NSCs in the DG divide to generate intermediate progenitor cells (IPCs), whose highly regulated dynamics of self-renewal or cell cycle exit decisions still remain poorly understood. Sox5 is a transcription factor (TF) essential for the establishment of adult NSCs, however, its potential role in Sox5 expressing IPCs during DG development remains unexplored. In this study, we demonstrate that conditional loss of Sox5 during embryonic development leads to critical alterations in cell proliferation and survival in IPCs. Specifically, following Sox5 loss, IPCs exhibit a shortening of S-phase duration in late postnatal and juvenile adult stages. Furthermore, these alterations in IPC cell cycle dynamics could be behind the defects in GN differentiation observed in Sox5-defective mice that ultimately leads to subtle morphological changes in DG architecture. Finally, we demonstrate that the additional loss of one Sox6 copy, a closely related TF to Sox5, lead to more profound disruptions in DG morphology than the one observed upon Sox5 loss. Overall, these findings point to a prominent role for Sox5 in combination with Sox6 in IPC cell cycle progression and GN maturation during postnatal DG development.
    Keywords:  Lamb-Shaffer syndrome; Sox5; Sox6; adult neurogenesis; cell cycle; hippocampus; neurogenesis; proliferation
    DOI:  https://doi.org/10.3389/fcell.2026.1876208
  2. CNS Neurosci Ther. 2026 Aug;32(8): e71040
    Chronic Smoking Impairs Glymphatic Transport and Cognitive Function in Adolescent Mice Through Cardiac, Vascular, and Perivascular Aquaporin-4 Mechanisms.
    Chuanxiang Lv, Chengyu Xia, Zean Li, Tao Liu, Zhuang Sha, Shiying Dong, Yu Qian, Mingqi Liu, Kang Zhang, Xinran Zhang, Rongcai Jiang, Li Bie.
       AIMS: Smoking significantly impairs cognitive function and is a major risk factor for dementia, particularly when initiated during adolescence, a critical period for brain development. The glymphatic system, which is thought to participate in metabolic waste clearance, has been implicated in maintaining cognitive health. This study investigates the effects of chronic smoking on glymphatic transport and its underlying mechanisms.
    METHODS: Glymphatic transport was assessed using immunofluorescence and two-photon microscopy, while phosphorylated tau accumulation in the dentate gyrus (DG) was examined via immunohistochemical staining. Synaptogenesis and neurogenesis in the hippocampal DG were analyzed using synaptophysin, PSD-95, doublecortin, and standard histological techniques. Cognitive function was measured through the Morris water maze (MWM) test and novel object recognition (NOR) tests, with cardiac function assessed by echocardiography.
    RESULTS: The findings indicate that chronic smoking leads to a duration-dependent disruption of glymphatic transport, resulting in the accumulation of phosphorylated tau in the hippocampal DG, reduced synaptogenesis and neurogenesis, and subsequent cognitive decline.
    CONCLUSION: This glymphatic dysfunction may be associated with impaired cardiac ejection, diminished arterial pulsatility, and loss of perivascular aquaporin-4 (AQP4), collectively contributing to smoking-related cognitive impairment.
    Keywords:  arterial pulsatility; chronic smoking exposure; cognitive impairment; glymphatic system; perivascular AQP4
    DOI:  https://doi.org/10.1002/cns.71040
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