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Recent Molecular Basis of Neurocognitive Mechanism

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 25 October 2025 | Viewed by 854

Special Issue Editor


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Guest Editor
Osher Center for Integrative Health, Vanderbilt University Medical Center, Nashville, TN 37203, USA
Interests: integrative medicine; neurophysiology; neuropsychiatry; omics

Special Issue Information

Dear Colleagues,

Molecular biology and neuroscience have been significantly advanced by the application of high-throughput omics sequencing and mass spectrometry technologies, such as proteomics, transcriptomics, genomics, metabolomics, lipidomics, and epigenomics. These interdisciplinary research efforts have led to the development of innovative methodologies, comprehensive multi-modal datasets, and valuable genotypic and phenotypic markers. They have also provided deeper insights into treatments, particularly concerning human brain function and cognitive dynamics. A notable example is the recently developed NeuroPro searchable database by Askenazi et al. (2023), which has identified 848 proteins consistently altered in neurodegeneration. This database can distinguish changes in specific proteins associated with synapse, vesicle, and lysosomal pathways in early-stage cognitive decline, as opposed to widespread maladaptive changes in mitochondrial-associated proteins observed in late-stage Alzheimer’s Disease. Complementary to this, data from Soldan et al. (2023) indicate that baseline levels of the synaptic protein NPTX2 in cerebral spinal fluid (CSF) can predict the onset of mild cognitive impairment. Another significant contribution comes from Darst et al. (2021), who presented a large longitudinal metabolomic dataset showing that specific plasma metabolites, such as the amino acid cysteine S-sulfate and the fatty acid erucate, are associated with age-related decline in executive functioning. These findings not only advance our understanding of the basic mechanisms underlying neurocognition, such as executive function, inhibitory control, language processing, learning, perception, and memory, but also highlight the translational potential for neurocognitive disorders. Identifying precursor markers of cognitive decline can inform neuroplastic interventions and precision neurorehabilitation. The evolving frontier in this field includes determining whether the most effective treatment strategies should target specific genotypes (e.g., gene therapy), underlying molecular pathways and dynamics (e.g., RNA splicing), or relevant neurocognitive functions and outcomes (e.g., neuro-training). This Special Issue invites original studies, reviews, and hypothesis/conceptual pieces that explore recent advances in human cognitive (dys)function from various neuro-molecular perspectives across clinical and/or adaptive contexts.

Dr. Poppy Schoenberg
Guest Editor

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Keywords

  • cognitive functioning
  • epigenomics
  • high-throughput omics
  • metabolomics
  • molecular pathways
  • multi-modal datasets
  • neurocognition
  • neurodegeneration
  • neurorehabilitation
  • proteomics
  • transcriptomics

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Published Papers (1 paper)

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Research

19 pages, 8963 KiB  
Article
A Chloroform Fraction Derived from Vitis vinifera Root Ethanol Extract Attenuates Lipopolysaccharide-Induced Inflammatory Responses and Cognitive Dysfunction in BV-2 Microglia Cells and C57BL/6J Mouse Model
by Yon-Suk Kim, Sang-Bong Lee, Shin-Il Kang, Woo-Jung Kim and Dong-Kug Choi
Int. J. Mol. Sci. 2025, 26(7), 3126; https://doi.org/10.3390/ijms26073126 - 28 Mar 2025
Viewed by 379
Abstract
This study aimed to investigate the inhibitory effect of the chloroform fraction (CF) from Vitis vinifera root extract on LPS-induced neuroinflammation in BV-2 microglia cells and a C57/BL6J mouse model. CF significantly suppressed LPS-induced proinflammatory cytokines, including nitric oxide (NO), tumor necrosis factor-α [...] Read more.
This study aimed to investigate the inhibitory effect of the chloroform fraction (CF) from Vitis vinifera root extract on LPS-induced neuroinflammation in BV-2 microglia cells and a C57/BL6J mouse model. CF significantly suppressed LPS-induced proinflammatory cytokines, including nitric oxide (NO), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) in BV-2 microglia cells. Mechanistically, CF inhibited LPS-induced activation of nuclear factor-κB (NF-κB) by blocking the p65 subunit and preventing the phosphorylation of NF-kappa-B inhibitor α (IκBα), while its effect was independent of the mitogen-activated protein kinase (MAPK) pathway. Furthermore, CF modulated the TRIF signaling pathway by regulating TANK-binding kinase 1 (TBK1) and interferon regulatory factor 3 (IRF3), which contributed to the suppression of inflammatory mediators in BV-2 microglia cells. In vivo, we evaluated the neuroprotective effects of CF against cognitive dysfunction and inflammatory responses in an LPS-induced mouse model. Our behavioral assessments, including the Morris water maze and Y-maze tests, demonstrated that CF alleviated LPS-induced spatial learning impairment and cognitive decline. Additionally, CF significantly reduced the levels of inflammatory cytokines in serum and inflammatory mediators proteins expression in whole brain in LPS-injected mice, suggesting a direct link between reduced inflammatory responses and improved cognitive function. These findings suggest that CF from V. vinifera root extract may serve as a potential therapeutic strategy for neurodegenerative diseases mediated by microglial activation, such as Alzheimer’s disease. Full article
(This article belongs to the Special Issue Recent Molecular Basis of Neurocognitive Mechanism)
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