Inflammation and Brain Diseases

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Medicinal Chemistry".

Deadline for manuscript submissions: closed (15 October 2023) | Viewed by 4284

Special Issue Editors


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Guest Editor
Department of Pharmacy, University of Pisa, 56126 Pisa, Italy
Interests: brain diseases; electrophysiology; epilepsy; cortical plasticity

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Guest Editor
Department of Pharmacy, University of Pisa, Via Bonanno 6, 56126 Pisa, Italy
Interests: amyloid proteins; medicinal chemistry; degenerative diseases; drug design; X-ray crystallography; chemical synthesis
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Associate Professor, Department of Pharmacy, University of Pisa, 56126 Pisa, Italy
Interests: medicinal chemistry; drug discovery; metalloenzyme inhibitors; neurodegenerative diseases; anticancer drugs; CNS agents; chemical synthesis; structure–activity relationship; natural products
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Inflammation is the common denominator of several CNS pathologies. It is now well-accepted that inflammatory pathways are involved in the pathogenesis of several neurodegenerative disorders, such as multiple sclerosis (MS), Parkinson’s disease (PD), and Alzheimer’s disease (AD), and they are known to be activated following neurologic infection, ischemic stroke, and traumatic brain injury. In addition, clinical observations and experimental findings support a link between inflammation and epilepsy. In the brain, the major players in the inflammatory response are resident cellular elements. Microglia and astrocytes are strongly activated in most neurodegenerative diseases and produce a variety of inflammatory mediators. Whether the neuroinflammatory reaction is beneficial or detrimental to disease progression is still a matter of debate. However, in recent decades, most findings have suggested that inflammation exacerbates the pathological manifestation of CNS diseases. This evidence has framed inflammation as a common target for a broad range of CNS diseases. Thus, anti-inflammatory agents could potentially be effective for different pathologies. Approved anti-inflammatory drugs, as well as innovative, multifunctional, and/or hybrid molecules, are fundamental tools both in elucidating pathological pathways of brain diseases and in mitigating disease progression.

This Special Issue aims to provide an overview of approved drugs exploited in brain diseases and to highlight state-of-the-art new compounds under study.

Dr. Chiara Cerri
Dr. Lidia Ciccone
Dr. Susanna Nencetti
Guest Editors

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Keywords

  • neuroinflammation
  • anti-inflammatory drugs
  • neurodegenerative disorders
  • epilepsy
  • drug design
  • computational methods
  • systemic inflammation

Published Papers (2 papers)

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Research

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15 pages, 3967 KiB  
Article
A Window to the Brain: The Retina to Monitor the Progression and Efficacy of Saffron Repron® Pre-Treatment in an LPS Model of Neuroinflammation and Memory Impairment
by Mattia Di Paolo, Francesca Corsi, Chiara Cerri, Silvia Bisti, Ilaria Piano and Claudia Gargini
Pharmaceuticals 2023, 16(9), 1307; https://doi.org/10.3390/ph16091307 - 15 Sep 2023
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Abstract
A mechanism shared by most neurodegenerative diseases, like Alzheimer’s disease (AD) and Parkinson’s disease (PD), is neuroinflammation. It has been shown to have a link between cognitive impairment and retinal function under neuroinflammatory conditions, confirming the essential role of the retina as a [...] Read more.
A mechanism shared by most neurodegenerative diseases, like Alzheimer’s disease (AD) and Parkinson’s disease (PD), is neuroinflammation. It has been shown to have a link between cognitive impairment and retinal function under neuroinflammatory conditions, confirming the essential role of the retina as a window to the brain. Here, we characterize a mouse model of LPS-induced neuroinflammation describing the parallel deterioration of both memory and visual function. Then, we demonstrate, using the Novel Object Recognition test (NOR) and electroretinogram (ERG) recordings, that preventive, chronic treatment with saffron Repron® is able to reduce the neuroinflammation process and prevent the impairment of both cognitive and visual function. The improvement in behavioral and visual function is confirmed by the pattern of expression of neuroinflammation-related genes and related proteins where pre-treatment with Repron® saffron presents a positive modulation compared with that obtained in animals treated with LPS alone. These results hold for retinal tissue and partially in the brain, where it appears that the onset of damage was delayed. This trend underlines the critical role of the retina as a most sensitive portion of the central nervous system to LPS-induced damage and could be used as a “sensor” for the early detection of neurodegenerative diseases such as Alzheimer’s. Full article
(This article belongs to the Special Issue Inflammation and Brain Diseases)
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17 pages, 1816 KiB  
Review
Role of MicroRNA-502-3p in Human Diseases
by Davin Devara, Yashmit Choudhary and Subodh Kumar
Pharmaceuticals 2023, 16(4), 532; https://doi.org/10.3390/ph16040532 - 02 Apr 2023
Cited by 4 | Viewed by 2406
Abstract
MicroRNAs (miRNAs) are non-coding RNAs that play a major role in gene regulation in several diseases. MicroRNA-502-3p (MiR-502-3p) has been previously characterized in a variety of human diseases such as osteoporosis, diabetes, tuberculosis, cancers, and neurological disorders. Our studies recently explored the new [...] Read more.
MicroRNAs (miRNAs) are non-coding RNAs that play a major role in gene regulation in several diseases. MicroRNA-502-3p (MiR-502-3p) has been previously characterized in a variety of human diseases such as osteoporosis, diabetes, tuberculosis, cancers, and neurological disorders. Our studies recently explored the new role of miR-502-3p in regulating synapse function in Alzheimer’s disease (AD). AD is the most common cause of dementia in elderly individuals. Synapse is the initial target that is hit during AD progression. The most common causes of synapse dysfunction in AD are amyloid beta, hyperphosphorylated tau, and microglia activation. MiR-502-3p was found to be localized and overexpressed in the AD synapses. Overexpression of miR-502-3p was correlated with AD severity in terms of Braak stages. Studies have shown that miR-502-3p modulates the glutaminergic and GABAergic synapse function in AD. The current study’s emphasis is to discuss the in-depth roles of miR-502-3p in human diseases and AD and the future possibilities concerning miR-502-3p as a therapeutic for AD treatment. Full article
(This article belongs to the Special Issue Inflammation and Brain Diseases)
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