bims-adhine Biomed News
on Adult hippocampal neurogenesis
Issue of 2026–08–16
nine papers selected by
Tamara J. Buijs, Universiteit van Amsterdam
  1. DGIST: A standardized image-based spatial quantification workflow for neurogenesis in the dentate gyrus.
  2. Δ9-Tetrahydrocannabinol Modulates Hippocampal Neurogenesis in Female Wistar Rats: Interaction with Estradiol.
  3. Nuclear distribution element-like 1 is associated with dentate gyrus remodeling after status epilepticus in a pilocarpine-induced mouse model.
  4. Electroacupuncture improves neurocognitive impairment induced by chronic sleep deprivation: an experimental study based on hippocampal neurogenesis and synaptic plasticity.
  5. Immature Neurons in the Postnatal Brain: Markers, Modulation, and Involvement in Normal and Aberrant Plasticity.
  6. Salidroside enhances hippocampal neurogenesis in a valproic acid-induced mouse model of autism by suppressing neuroinflammation.
  7. The effects of blast-induced traumatic brain injury on brain cellular mechanics and differentiation.
  8. Ivermectin impairs memory retrieval performance by B6 nestin-cre mice.
  9. Energetic crisis, mitochondrial vulnerability and disruption of lactate shuttle in Alzheimer's disease.
  1. Adv Biol Regul. 2026 Aug 04. pii: S2212-4926(26)00030-8. [Epub ahead of print]101 101173
    DGIST: A standardized image-based spatial quantification workflow for neurogenesis in the dentate gyrus.
    Jinhee Lee, Wonyoung Lee, Yoichi Kosodo.
      The adult hippocampus generates new neurons in the dentate gyrus (DG), where neural stem cells (NSCs) in the subgranular zone differentiate into neuronal and astroglial lineages. Accurate quantification of adult NSCs is critical for assessing neurogenic potential, yet most current methods rely on manual, density-based measurements in limited regions of the DG. These approaches may introduce bias due to morphological variability among tissue sections. To overcome these challenges, we developed the Dentate Gyrus Image-based Spatial quantification Tool (DGIST), an ImageJ/Fiji-based workflow that integrates BioVoxxel and MorphoLibJ plug-ins for cell-based quantification throughout the entire DG. Applied to in vivo datasets, DGIST quantifies age-dependent changes in marker-defined NSC and astroglial populations. Our results demonstrate that DGIST provides a reproducible method for quantifying marker-defined populations in the adult neurogenic niche.
    Keywords:  Adult neurogenesis; Dentate gyrus; Hippocampus; ImageJ; Neural stem cells; Quantification
    DOI:  https://doi.org/10.1016/j.jbior.2026.101173
  2. Neurochem Res. 2026 Aug 08. pii: 234. [Epub ahead of print]51(4):
    Δ9-Tetrahydrocannabinol Modulates Hippocampal Neurogenesis in Female Wistar Rats: Interaction with Estradiol.
    Duarte R Carvalhinho, Sandra I Marques, Sandra Leal, Bruno M Fonseca, José P Andrade, Susana I Sá.
      The endocannabinoid system (ECS) plays a key role in regulating neurogenesis and inflammatory processes in the brain. The increasing prevalence of Cannabis use among women highlights the importance of understanding sex-specific effects of cannabinoids, particularly in the context of hormonal interactions. This study aimed to investigate the effects of delta-9-tetrahydrocannabinol (THC) and estradiol benzoate (EB) on adult hippocampal neurogenesis (AHN) and inflammation in ovariectomized female Wistar rats. Sixteen rats were allocated to four experimental groups receiving THC, EB, both treatments, and vehicle. Immunohistochemical analyses were conducted to evaluate markers of proliferation (Ki-67), neurogenesis (doublecortin and PSA-NCAM), cannabinoid receptor expression (CB1), and inflammation (COX-2 and TNF-α) in the hippocampal formation. The administration of THC significantly increased Ki-67 immunoreactivity, suggesting enhanced cell proliferation. A trend toward increased doublecortin expression was observed, particularly in EB-treated animals. THC also modulated CB1 receptor expression, with significant increases in the dentate gyrus and hilus following combined THC and EB treatment. Furthermore, THC reduced inflammatory markers, with region-dependent decreases in COX-2 and TNF-α expression. These findings indicate that THC influences markers associated with hippocampal cell proliferation, neurogenesis, cannabinoid signaling and inflammation in female rats, and that some of these effects depend on estradiol status. The interaction between cannabinoids and gonadal hormones may represent an important mechanism underlying sex-specific neurobiological responses and suggests potential targets for therapeutic intervention in neuropsychiatric disorders.
    Keywords:  Endocannabinoid system; Estradiol; Female rats; Hippocampal neurogenesis; Inflammation; THC
    DOI:  https://doi.org/10.1007/s11064-026-04857-w
  3. Neuroscience. 2026 Aug 13. pii: S0306-4522(26)00538-5. [Epub ahead of print]
    Nuclear distribution element-like 1 is associated with dentate gyrus remodeling after status epilepticus in a pilocarpine-induced mouse model.
    Jing Xu, Lin Zhu, Lu Chen, Xiaoyu Du, Yue Xu, Qian Wu.
      Structural remodeling of the dentate gyrus is a hallmark of temporal lobe epilepsy (TLE), yet the underlying molecular mechanisms remain incompletely understood. Nuclear distribution element-like 1 (Ndel1), a cytoskeleton-associated protein involved in neuronal migration and dendritic development, has not been characterized in dentate gyrus remodeling during epileptogenesis. Here, we investigated region- and cell-type-specific alterations in Ndel1 expression in a pilocarpine-induced mouse model of TLE and examined the effects of adeno-associated virus (AAV)-mediated Ndel1 expression on structural remodeling. Immunofluorescence was used to define Ndel1 localization across neural stem cells, granule lineage cells, mature neurons, and astrocytes, and dendritic architecture was assessed using Golgi staining and Sholl analysis. Total hippocampal Ndel1 expression increased after status epilepticus, whereas Ndel1-positive cells decreased selectively in the subgranular zone but increased among granule lineage cells in the hilus. Ndel1 was preferentially expressed in BLBP-positive neural stem cells and mature neurons, but not in neuroblasts. Activated astrocytic processes exhibited increased spatial association with Ndel1-positive cells during early remodeling. Ndel1 overexpression was associated with partial normalization of neuronal marker distribution, increased dendritic spine density, and reduced dendritic branching complexity. These findings suggest that Ndel1 is associated with region- and lineage-specific structural remodeling in the dentate gyrus during epileptogenesis.
    Keywords:  Adult neurogenesis; Dendritic remodeling; Dentate gyrus; Ndel1 (Nuclear distribution element-like 1); Status epilepticus; Temporal lobe epilepsy
    DOI:  https://doi.org/10.1016/j.neuroscience.2026.08.009
  4. Front Hum Neurosci. 2026 ;20 1857669
    Electroacupuncture improves neurocognitive impairment induced by chronic sleep deprivation: an experimental study based on hippocampal neurogenesis and synaptic plasticity.
    Jianli Wu, Jiajing Sun, Mengdi Li, Hao Wang, Geling Lu, Chen Guo, Kunping Jia, Miao Zhang.
       Objective: Normal sleep rhythms are crucial for hippocampus-dependent advanced cognitive functions. Chronic sleep deprivation (CSD) impairs hippocampal neurogenesis and structure, leading to neurocognitive deficits. Electro-nape-acupuncture (ENA) at bilateral Fengchi (GB20) and Gongxue (Extra) is a specialized acupuncture technique for treating insomnia, amnesia, and other brain-originated diseases. This study aims to investigate whether ENA improves CSD-induced cognitive impairment by regulating neurogenesis and synaptic plasticity in the hippocampus.
    Methods: The modified multi-platform water environment method was used to establish the CSD model. Electroacupuncture or sham electroacupuncture was used to treat bilateral cervical acupoints (Fengchi and Gongxue) for 20 min, once a day for 14 days. The Morris water maze experiment evaluated spatial learning and memory in rats, and the new object recognition experiment evaluated recognition memory. Immunofluorescence (IF) staining and Western Blot (WB) were used to detect the expression levels of the hippocampal neurogenesis markers, doublecortin (DCX) and Ki-67. Golgi-Cox staining and transmission electron microscopy were used to observe the changes in neurons and synaptic plasticity in the dentate gyrus (DG) of the hippocampus.
    Results: Neurocognitive impairment induced by CSD is associated with abnormal changes in hippocampal neurogenesis and synaptic plasticity. The results of IF and WB showed that the protein expressions of DCX and Ki-67 in the hippocampus of CSD rats were significantly decreased. Transmission electron microscopy revealed that in the DG region of the hippocampus of CSD rats, the synaptic density and the thickness of the postsynaptic density membrane decreased, while the synaptic cleft width increased. Golgi staining showed that the density of dendritic spines in the DG area of the hippocampus in CSD rats decreased significantly, especially mushroom-shaped dendritic spines. ENA can enhance spatial learning and memory, as well as recognition memory, induced by CSD, and effectively reverse the abnormal changes in neurogenesis and synaptic plasticity in the DG region of the hippocampus.
    Conclusion: In male Wistar rats, ENA improves neurocognitive function by promoting neurogenesis in the hippocampal dentate gyrus and restoring synaptic plasticity, thereby reconstructing neural memory circuits. ENA therapy offers a new strategy for treating cognitive impairments related to chronic sleep deprivation in males, and holds potential significance for the clinical management of cognitive impairment diseases.
    Keywords:  chronic sleep deprivation; cognitive impairment; electroacupuncture; hippocampal neurogenesis; synaptic plasticity
    DOI:  https://doi.org/10.3389/fnhum.2026.1857669
  5. Int J Mol Sci. 2026 Jul 27. pii: 6696. [Epub ahead of print]27(15):
    Immature Neurons in the Postnatal Brain: Markers, Modulation, and Involvement in Normal and Aberrant Plasticity.
    Viacheslav Riga, Victor Aniol, Natalia Gulyaeva.
      Cortical immature neurons (cINs) represent a unique population of prenatally generated, non-dividing neurons that maintain an immature phenotype, characterized by doublecortin (DCX) and polysialylated neural cell adhesion molecule (PSA-NCAM) expression, into adulthood. Unlike canonical adult neurogenesis involving continuous neuron generation from stem cell niches, cINs constitute a distinct form of structural plasticity termed "neurogenesis without division". This review comprehensively examines the molecular markers, morphological diversity, developmental origins, and maturation trajectories of cINs across species. We highlight the striking inverse interspecies relationship between cIN abundance and canonical adult neurogenesis, reflecting distinct biophysical and structural shifts in neural plasticity mechanisms across mammalian lineages. Furthermore, we discuss factors modulating cIN phenotype, including neurotransmitter systems, stress, sensory experience, and aging. Clinical evidence implicating cIN alterations in temporal lobe epilepsy, traumatic brain injury, and stroke is evaluated, revealing potential roles in both pathological circuit remodeling and endogenous repair. Critical gaps remain regarding the molecular programs maintaining immaturity, differentiation triggers, and the functional consequences of circuit integration. Understanding cIN biology offers new perspectives on cortical plasticity and may inform therapeutic strategies targeting endogenous cellular reserves for brain repair.
    Keywords:  DCX; PSA-NCAM; epilepsy; evolution; neocortex; neurogenesis; neuronal development; neuronal precursors; piriform cortex; structural plasticity
    DOI:  https://doi.org/10.3390/ijms27156696
  6. Int Immunopharmacol. 2026 Aug 04. pii: S1567-5769(26)01041-6. [Epub ahead of print]187 117195
    Salidroside enhances hippocampal neurogenesis in a valproic acid-induced mouse model of autism by suppressing neuroinflammation.
    Xinyi Wang, Rui Li, Yanna Li, Di Wang, Yulong Cai, Xinfeng Liu.
       OBJECTIVE: Neuroinflammation plays a pivotal role in the pathogenesis of autism spectrum disorder (ASD) and represents a potential therapeutic target. Salidroside (SLDS), a bioactive compound isolated from Rhodiola rosea L., exhibits potent anti-inflammatory and neuroprotective effects in various neurological disorders; however, its therapeutic efficacy in ASD remains to be fully established. This study investigated whether SLDS ameliorates autism-like behaviors and hippocampal neuroinflammation in a valproic acid (VPA)-induced mouse model.
    METHODS: A total of 92 male C57BL/6 J mice were randomly assigned to four groups (n = 23 per group). Mice received a subcutaneous injection of VPA or saline on postnatal day 14 (P14), followed by intraperitoneal administration of SLDS or saline from postnatal day 28 (P28) for seven consecutive days. Behavioral assessments were conducted at 8 weeks of age. Hippocampal neuroinflammation, microglial polarization, and neurogenesis were analyzed by molecular, immunofluorescence, and histological techniques.
    RESULTS: VPA-exposed mice exhibited social interaction deficits, increased repetitive behaviors, elevated levels of pro-inflammatory cytokines, upregulated expression of inflammation-related proteins, microglial activation, and impaired hippocampal neurogenesis. SLDS treatment significantly attenuated these VPA-induced abnormalities.
    CONCLUSION: Collectively, these findings suggest that SLDS represents a promising therapeutic candidate for ASD by mitigating neuroinflammation and restoring hippocampal function. Nevertheless, given that these observations are derived from preclinical models, further validation in translationally relevant experimental systems and clinical investigations is warranted before extrapolation to human therapeutic applications.
    Keywords:  Autism spectrum disorder; Hippocampus; Neurogenesis; Neuroinflammation; Salidroside; Valproic acid
    DOI:  https://doi.org/10.1016/j.intimp.2026.117195
  7. PLoS One. 2026 ;21(8): e0355739
    The effects of blast-induced traumatic brain injury on brain cellular mechanics and differentiation.
    Nabila Masud, Catherine Fonder, Bridget McGovern, Md Hasibul Hasan Hasib, William J Jackson, Dulce C Resendiz, Carley Rivers, Sarah A Bentil, Donald S Sakaguchi, Anwesha Sarkar.
      Blast-induced traumatic brain injury (bTBI) causes significant disruptions in cellular and subcellular structures within the central nervous system (CNS) when an extremely large force is applied. The corresponding changes in biomechanical properties and cellular functionalities of neuronal and glial cells due to bTBI remain largely unexplored. In this work, high blast overpressures (BOPs) of 14.5 psi (single shockwave) and 29.0 psi (double shockwave) were applied to adult hippocampal progenitor cells (AHPCs) in two different directions (overpressure applied from 'top-to-bottom' and 'bottom-to-top' direction on the cell culture petridish). The resultant alterations in structural, nanomechanical, and viscoelastic properties as well as cellular survival, proliferation, and differentiation were analyzed using atomic force microscopy (AFM) and immunocytochemistry (ICC). Double shockwave exposure from 'bottom-to-top' direction yielded reduced Young's modulus, surface roughness, and viscosity, causing significant actin cytoskeletal disruptions compared to 'top-to-bottom' direction. ICC results demonstrated that double shockwave exposure from 'top-to-bottom' direction caused populations of oligodendrocytes and immature neurons to decrease, while 'bottom-to-top' double shockwave exposure caused an increase in the percentage of immature neurons as shown by increased TuJ1-immunoreactivity which is interpreted as evidence that cells have committed to a neuronal lineage and entered an immature/early neuronal stage. These findings emphasize the interplay among cellular differentiation, mechanics, and resilience of neuronal and glial cells to trauma in bTBI aftermath.
    DOI:  https://doi.org/10.1371/journal.pone.0355739
  8. Neurobiol Learn Mem. 2026 Aug 12. pii: S1074-7427(26)00077-8. [Epub ahead of print] 108206
    Ivermectin impairs memory retrieval performance by B6 nestin-cre mice.
    Lucia Schoderboeck, Shane M Ohline, Louise van der Salm, Hollie E Wicky, Stephanie M Hughes, Wickliffe C Abraham.
      The role of adult-born neurons in the hippocampal dentate gyrus and its significance in memory processes is a field of high interest. To add to this literature, we investigated the feasibility of ivermectin-based chemogenetic manipulation of recently born neurons in the hippocampus in altering spatial and contextual memory retrieval. The adult-born neurons in male mice were targeted using a nestin-cre mouse model, employing lentivirus-mediated transduction of inhibitory chloride channel constructs sensitive or insensitive to ivermectin in order to be able to silence them during different developmental stages. Two mouse age groups were compared: 5 weeks and 5 months old at the time of lentivirus injection. Behavioural assessments involving the Morris water maze and contextual fear conditioning were conducted. Unexpectedly, ivermectin administration alone led to apparent memory impairments regardless of the virus construct, confounding behavioural test outcomes. This study highlights the challenge of distinguishing specific effects of targeting adult-born neuronal activity from nonspecific effects of ivermectin on cognition.
    Keywords:  Chloride channel; Fear conditioning; Hippocampus; Ivermectin; Neurogenesis; Spatial memory
    DOI:  https://doi.org/10.1016/j.nlm.2026.108206
  9. Int Rev Neurobiol. 2026 ;pii: S0074-7742(26)00040-1. [Epub ahead of print]188 67-89
    Energetic crisis, mitochondrial vulnerability and disruption of lactate shuttle in Alzheimer's disease.
    Gowsika Baskar, Mahesh Kandasamy.
      Alzheimer's disease (AD) has traditionally been characterized by amyloid-beta (Aβ) plaques and neurofibrillary tangles. Emerging evidence reveals that metabolic dysfunction represents a key pathological feature central to disease progression. Mitochondrial dysfunction in AD leads to impaired electron transport chain activity and reduced level of adenosine triphosphate (ATP) synthesis, preceding neurodegeneration and structural abnormalities in cognitive centres of the brain. Early glucose hypometabolism and lactate deprivation or interference with their utilization represent a primary bioenergetic failure driving mitochondrial dysfunction and neuroinflammation prior to the clinical manifestation of AD. While the brain relies on lactate as a prominent energy substrate, astrocytic metabolic defects lead to impaired neuronal energy homeostasis, thereby promoting neurodegeneration. In turn, this metabolic uncoupling could also be associated with defects in regenerative mechanisms by impairing adult neurogenesis in the hippocampus due to energy deprivation, accounting for memory deficits. This chapter discusses the evidence for the energetic crisis in AD, focusing on the disruption of the astrocyte-neuron lactate shuttle (ANLS), hypometabolism of glucose, and mitochondrial vulnerability, as interconnected pathogenic mechanisms. We emphasise cerebral bioenergetic metabolic failure as a central driver of cognitive decline, arising from irreversible reactive gliosis and neuroblastosis mechanisms and highlight various therapeutic options, including restoration of ANLS to mitigate the pathogenesis and memory loss in AD.
    Keywords:  Alzheimer's disease; Bioenergetic crisis; Lactate shuttle; Mitochondrial defects; Neurogenesis; Neuroinflammation
    DOI:  https://doi.org/10.1016/bs.irn.2026.05.012
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