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Neuropharmacology and Brain Physiology: From Molecular Mechanisms to Medicines Application

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Pharmacology".

Deadline for manuscript submissions: 31 January 2025 | Viewed by 574

Special Issue Editor


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Guest Editor
Department of Neurosciences, Psychology, Drug Research and Child Health (NEUROFARBA)—Pharmacology and Toxicology Session, University of Florence (UNIFI), 50139 Florence, Italy
Interests: neuropharmacology; neuroscience; drug discovery; brain histamine; brain carbonic anhydrases; oxytocin
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Special Issue Information

Dear Colleagues,

Neuropharmacology is a dynamic field that has seen significant advancements in recent years. Research has uncovered intricate details about the neurotransmitter systems, receptor dynamics, and intracellular signaling pathways that regulate neuronal activity and synaptic plasticity. For instance, studies on the dopaminergic system have elucidated its role in reward processing and motor control, while investigations into glutamatergic and GABAergic systems have shed light on excitatory and inhibitory balance in the brain. Moreover, the molecular mechanisms underlying neuropsychiatric and neurodegenerative disorders, such as Alzheimer's disease, Parkinson's disease, depression, and schizophrenia, have been increasingly delineated, revealing potential targets for pharmacological intervention.

This Special Issue will highlight the translational aspect of neuropharmacology by presenting research on the development of novel pharmacological agents and therapeutic strategies aimed at modulating these molecular targets. Through this Special Issue, we will bridge the gap between basic molecular research and clinical application, fostering a deeper understanding of how molecular mechanisms can be harnessed to develop effective treatments for brain disorders. Researchers are invited to submit original research articles, reviews, and perspectives that contribute to this dynamic and evolving field.

Dr. Gustavo Provensi
Guest Editor

Manuscript Submission Information

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Keywords

  • neuropsychopharmacology
  • neurotransmitters
  • neuropeptides
  • receptor proteins
  • agonist
  • competitive antagonist
  • non-competitive antagonist

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Published Papers (1 paper)

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Research

15 pages, 3119 KiB  
Article
Assessment of Modified Citrus Pectin’s Effects on Dementia in the Scopolamine-Induced Alzheimer’s Model in Adult Male Wistar Rats
by Jale Akgöl, Özden Kutlay, Arzu Keskin Aktan and Fatma Fırat
Curr. Issues Mol. Biol. 2024, 46(12), 13922-13936; https://doi.org/10.3390/cimb46120832 - 11 Dec 2024
Viewed by 365
Abstract
Modified citrus pectin (MCP) modulates galectin-3, a key player in neuroinflammation linked to Alzheimer’s disease. By inhibiting galectin-3, MCP reduces the brain’s inflammatory response and may alleviate cognitive decline. This study examines MCP’s impact on neuroinflammation, cognitive function, and its role in galectin-3 [...] Read more.
Modified citrus pectin (MCP) modulates galectin-3, a key player in neuroinflammation linked to Alzheimer’s disease. By inhibiting galectin-3, MCP reduces the brain’s inflammatory response and may alleviate cognitive decline. This study examines MCP’s impact on neuroinflammation, cognitive function, and its role in galectin-3 inhibition in a dementia model. Male Wistar rats were assigned to four groups: control (n = 6), scopolamine (SCP) (n = 7), SCP + MCP (n = 7), and MCP only (n = 7). MCP was administered orally at 100 mg/kg/day via drinking water for six weeks. SCP was injected intraperitoneally at 1 mg/kg for seven days to induce an Alzheimer’s-type dementia model. The researchers assessed cognitive performance through the Morris Water Maze (MWM) test. After behavioral tests, blood and brain tissues, including the hippocampus, were collected and stored at −80 °C for analysis. Immunohistochemistry was used to evaluate superoxide dismutase (SOD) activity, malondialdehyde (MDA) levels, brain-derived neurotrophic factor (BDNF), and inflammatory markers (IL-1β, IL-6, TNF-α, and galectin-3). The data were analyzed with SPSS 22. SCP treatment increased lipid peroxidation (MDA) and elevated inflammatory markers (TNF-α, IL-6, and galectin-3), while reducing BDNF and impairing spatial memory. Co-administering MCP with SCP significantly reduced TNF-α, IL-6, and galectin-3 levels; increased BDNF; and improved memory performance. Although MCP did not lower MDA levels, it boosted SOD activity, suggesting antioxidant effects. Modified citrus pectin (MCP) alleviated cognitive impairments and reduced neuroinflammation in Alzheimer’s-type dementia by inhibiting galectin-3. MCP also exhibited antioxidant potential, underscoring its therapeutic promise for neurodegenerative diseases. Full article
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