bims-adhine 2026-08-30 papers

Int J Mol Sci. 2026 Aug 17. pii: 7342. [Epub ahead of print]27(16):

Potential Role of Sphingosine-1-Phosphate and Its Receptors in the Reparative Processes of the Adult Brain.

Uliana A Gutner, Maria A Shupik, Alice Alessenko.

This review highlights the main aspects of the involvement of sphingosine-1-phosphate (S1P) metabolism in the reparative processes of the adult brain, including neurogenesis, oligodendrogenesis and angiogenesis, which are necessary for the normal functioning of the central nervous system. Neurogenesis is a complex, multifactorial, and multi-stage process of formation of neurons and neuroglial cells from neural stem cells. Neurotrophic factors, such as brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF) and fibroblast growth factor (FGF), play a special role in the regulation of neurogenesis. The fine regulation of neurogenesis, which occurs at all its stages, includes the molecular mechanisms of cellular signaling mediated by S1P and its receptors. In particular, S1P and its receptors affect adult neurogenesis at multiple stages: activation of S1P receptors induces neuroblast proliferation, migration, and morphological changes. Special attention is paid to the interaction of S1P and its receptors with the cellular environment (astrocytes, endothelial cells, and ependyma) of the neurogenic niche and the relationship between S1P metabolism and the expression of neurotrophins, which suggests a key role of S1P in regulating the environment of the neurogenic niche.

Keywords: angiogenesis; neurogenesis; neurogenic niche; neurotrophins; oligodendrogenesis; sphingosine-1-phosphate; sphingosine-1-phosphate receptors

DOI: https://doi.org/10.3390/ijms27167342

iScience. 2026 Sep 18. 29(9): 117207

Physical activity stimulates neurogenesis via sensory neuron activity in postembryonic zebrafish.

Shelby Sherlock, Lauren Appel, Zachary Hall, Anna Phan.

Physical exercise induces neurogenesis in adult and developing animal brains, but how movement promotes neurogenesis remains unclear. Here, we use two independent methods for immobilization, a physical barrier (gel matrix) or a genetic manipulation (CRISPR-Cas9 mutation of chrna1), to completely immobilize zebrafish larvae during postembryonic development. Both immobilization methods result in smaller brains, reduced brain cell proliferation, and accelerated neuronal differentiation. Conversely, exercised fish in a swim tunnel had larger brains, increased brain cell proliferation, and delayed neuronal differentiation. Interestingly, these effects of exercise could be mimicked by increasing neural activity pharmacologically using GABAA receptor antagonist pentylenetetrazol, or by artificially activating the dorsal root ganglia (DRG) sensory neurons, which increases swimming. Both promote cell proliferation and delayed neuronal differentiation. Finally, we dissociate the role of muscle contractions from neural activity by artificially activating the DRG neurons in CRISPR-chrna1 mutants, completely reversing neurogenesis defects that result from muscle paralysis.

Keywords: exercise; neurodevelopmental disorders; neurogenesis; synaptic plasticity

DOI: https://doi.org/10.1016/j.isci.2026.117207

Biochem Biophys Res Commun. 2026 Aug 18. pii: S0006-291X(26)01220-9. [Epub ahead of print]834 154456

Low expression of PDGFR-β impairs the blood-brain barrier and accelerates cellular aging in the hippocampal region.

Haichao Chen, Le Zhang, Xiaoling Zhu, Cheng Gu, Fulin Gao.

BACKGROUND: Platelet-Derived Growth Factor Receptor Beta (PDGFR-β), a key marker of cerebrovascular pericytes, plays a crucial role in regulating pericyte function and maintaining the stability of the blood-brain barrier (BBB). Recent studies suggest that abnormalities in the PDGFR-β signaling pathway may be closely associated with the onset and progression of neurodegenerative diseases. However, the causal relationship and specific mechanisms by which PDGFR-β gene deficiency directly leads to systemic pathological alterations in the hippocampal microenvironment, subsequently causing impaired neurogenesis and cellular senescence, remain unclear.
METHODS: Using PDGFR-β heterozygous knockout (PDGFR-β+/-) mice, we systematically examined pericyte coverage, BBB integrity, cellular senescence markers, and hippocampal neurogenesis.
RESULTS: PDGFR-β ± mice exhibited significant pericyte loss, reduced tight junction proteins, impaired vascular basement membrane, and increased BBB permeability in the hippocampus. These changes were accompanied by elevated DNA damage response, increased p16-positive senescent cells, and markedly reduced numbers of SOX2-positive neural stem/progenitor cells and DCX-positive immature neurons in the hippocampus.
CONCLUSION: Our findings establish that PDGFR-β haploinsufficiency drives pericyte loss and BBB breakdown, leading to hippocampal cellular senescence and impaired neurogenesis. This highlights vascular instability as a key driver of brain aging and positions pericyte dysfunction as a critical link between genetic susceptibility and age-related cognitive decline.

Keywords: Aging; Blood-brain barrier; Neurogenesis; Pericytes; Platelet-derived growth factor receptor β

DOI: https://doi.org/10.1016/j.bbrc.2026.154456

STAR Protoc. 2026 Aug 26. pii: S2666-1667(26)00456-9. [Epub ahead of print]7(3): 104803

Protocol for functional characterization of adult hippocampal neural precursor cells under demyelinating injury conditions in mice.

Shiva Nemati, Soheila Karimi-Abdolrezaee.

Adult hippocampal neural precursor cells (Hip-NPCs) are highly influenced by brain injury and diseases. Investigating the properties of Hip-NPCs is important for determining their reparative response. Here, we present a protocol for the functional characterization of Hip-NPCs under physiological and demyelinating conditions in adult mice. We describe steps for assessing of Hip-NPC self-renewal, activation state, proliferation, metabolism, and tri-lineage fate commitment. This workflow enables systematic evaluation of how pathological conditions and therapeutic interventions alter Hip-NPC functional states and adaptive responses. For complete details on the use and execution of this protocol, please refer to Nemati et al.1.

Keywords: Cell Biology; Neuroscience; Stem Cells

DOI: https://doi.org/10.1016/j.xpro.2026.104803