Advanced Research in Neurogenesis and Neuroinflammation

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: 15 December 2025 | Viewed by 1655

Special Issue Editor


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Guest Editor
Department of Anatomy and Cell Biology, College of Medicine, The University of Illinois at Chicago, Chicago, IL 60612, USA
Interests: cellular and molecular neuroscience; neurogenesis; neurodegeneration; neuroinflammation

Special Issue Information

Dear Colleagues,

Neurogenesis refers to the process by which neural stem cells (NSCs) go through multiple stages of proliferation and differentiation, resulting in the generation of new neurons within the brain. These newly formed neurons integrate into the neural networks, playing a crucial role in the management of various brain functions such as learning and memory. The phenomenon of adult neurogenesis introduces a unique type of plasticity to the brain, enabling it to adapt over time. However, the generation of new neurons tends to decrease with age and is influenced by a range of intrinsic and extrinsic factors such as genetics, epigenetics, age, physical activity, dietary habits, sleep quality, sex hormones, and life experiences. An impaired capacity for generating new neurons has been associated with cognitive impairments in several neurodegenerative conditions. Inflammation is another significant key factor affecting altered neurogenesis. While short-term inflammation may be advantageous, chronic or excessive neuroinflammation can hinder neurogenesis. Importantly, neuroinflammation, propelled by various immune components like activated glial cells, cytokines, chemokines, and reactive oxygen species, can influence every aspect of adult neurogenesis, such as cell proliferation, differentiation, migration, survival of newly formed neurons, maturation, synaptogenesis, and neuritogenesis. The relationship between neuroinflammation and neurogenesis suggests that inflammation may affect both the development and functionality of new neurons. To create effective therapeutic strategies and innovative methods aimed at adjusting these two processes to combat neurodegeneration, a deeper understanding of the interactions between changed neurogenesis and neuroinflammation is essential.

This Special Issue will focus on the exploration of different aspects of neurogenesis, ranging from molecular levels to behavioral implications, alongside its connection with neuroinflammation. It encompasses both in vitro and in vivo research examining the interplay between neurogenesis and neuroinflammation. Contributions from diverse research domains, including disease modeling, human neuropathology, biochemical, molecular, and clinical investigations, as well as genomics, proteomics, and therapeutic interventions, are encouraged.

We look forward to receiving your contributions.

Dr. Muskan Gupta
Guest Editor

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Keywords

  • neurogenesis
  • neuroinflammation
  • neurodegeneration
  • neurodegenerative diseases
  • cognitive functions

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Published Papers (2 papers)

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Research

21 pages, 3330 KB  
Article
Neuronal Primary Cilia Mediate Noggin Release to Enable Extracellular Signaling
by Sara R. Dunlop, Justin A. Geier, Chian-Yu Peng and John A. Kessler
Cells 2025, 14(20), 1607; https://doi.org/10.3390/cells14201607 - 16 Oct 2025
Viewed by 453
Abstract
The primary cilium is generally viewed as a sensory organelle that transduces chemical and mechanical stimuli from the environment. In the adult hippocampus, primary cilia mediate the effects of sonic hedgehog (Shh) and other signals on neurogenesis and hippocampal function, and loss of [...] Read more.
The primary cilium is generally viewed as a sensory organelle that transduces chemical and mechanical stimuli from the environment. In the adult hippocampus, primary cilia mediate the effects of sonic hedgehog (Shh) and other signals on neurogenesis and hippocampal function, and loss of cilia leads to cognitive and behavioral deficits. The secreted peptide noggin is a bone morphogenetic protein (BMP) antagonist and plays a critical role in regulating adult hippocampal neurogenesis (AHN) and hippocampus-dependent behavior. Here, we show that noggin is expressed by mature granule cell neurons, that it is apically targeted and localized intracellularly near the pocket region of primary cilia, and that cilia regulate noggin release through Shh and somatostatin (SST) pathways. Further, granule cell activation modulates noggin dynamics both in vitro and in vivo. Together, these findings demonstrate synergy between Shh and noggin and the positive regulatory action of neuronal activity on regulating BMP antagonism within the neurogenic niche. Thus, the primary cilium is not only an organelle that transduces signals to neurons but also one that mediates extracellular signaling. Significance statement: Primary cilia are organelles that protrude from the surface of most vertebrate cell types. Defects in primary ciliary structure and function are associated with human disease. Primary cilia are generally viewed as exclusively sensory organelles that respond to environmental signals to regulate both cell development and adult cell function. This study demonstrates that the primary cilia in hippocampal granule cell neurons mediate the release of the BMP antagonist, noggin. These observations expand the current understanding of ciliary signaling and may inform future studies exploring the connection between hippocampal activity and cognition in ciliopathies. Full article
(This article belongs to the Special Issue Advanced Research in Neurogenesis and Neuroinflammation)
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13 pages, 1941 KB  
Article
When Two Worlds Collide: The Contribution and Association Between Genetics (APOEε4) and Neuroinflammation (IL-1β) in Alzheimer’s Neuropathogenesis
by Jagadeesh Narasimhappagari, Ling Liu, Meenakshisundaram Balasubramaniam, Srinivas Ayyadevara and W. Sue T. Griffin
Cells 2025, 14(15), 1216; https://doi.org/10.3390/cells14151216 - 7 Aug 2025
Viewed by 919
Abstract
Introduction: Here we consider the collision of a genetic factor and an essential instigator in Alzheimer’s neuropathogenesis: (i) the Alzheimer’s gene (APOEε4), which downregulates lysosomal autophagy and induces synthesis of (ii) the instigator, interleukin-1β (IL-1β), which drives synthesis of βAPP for Aβ plaques [...] Read more.
Introduction: Here we consider the collision of a genetic factor and an essential instigator in Alzheimer’s neuropathogenesis: (i) the Alzheimer’s gene (APOEε4), which downregulates lysosomal autophagy and induces synthesis of (ii) the instigator, interleukin-1β (IL-1β), which drives synthesis of βAPP for Aβ plaques and of MAPKp38 for phosphorylation of tau for formation of neurofibrillary tangles (NFTs), the two cardinal features of AD. Methods: RT-PCR, immunoblotting and immunohistochemistry techniques were used to assess the levels of IL-1β and its signaling cascade in ADε4,4, ε3,3, and age-matched controls (AMC3,3) in hippocampal regions of the brain. Results: IL-1β and its downstream signaling proteins TLR-2, MyD88, NFκB, COX-1, and COX-2 were greater in tissues from ADε4,4 than ADε3,3 or AMC3,3. Cathepsin B, D, and L levels, which play a pivotal role and are necessary for lysosomal autophagy, were lower in ADε4,4 than in ADε3,3 or AMC ε3,3. IL-1β and its downstream signaling cascade TLR-2, MyD88, NFκB, COX-1, and COX-2 expression levels were high in SH-SY5Y and T98G cells transfected with APOεE4. Conclusions: APOEε4 causes Alzheimer’s by downregulating autophagy, thus inducing IL-1β for Aβ plaque and neurofibrillary tangle formation. Full article
(This article belongs to the Special Issue Advanced Research in Neurogenesis and Neuroinflammation)
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