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Drug Development for Neurodegenerative Diseases
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Drug Development for Neurodegenerative Diseases

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Medicinal Chemistry".

Deadline for manuscript submissions: closed (31 January 2023) | Viewed by 18575

Special Issue Editor

Prof. Dr. Zhongzhen Zhou

E-Mail Website
Guest Editor
School of Pharmaceutical Sciences, Southern Medical University, Guangzhou, China
Interests: drug design; drug synthesis; neurodegenerative diseases

Special Issue Information

Dear Colleagues,

Neuropsychiatric disorders such as Parkinson's disease, schizophrenia, depression, and dementia are the most frequent diseases with a substantial loss of productivity and life quality and significant morbidity. Thus, continued efforts for discovering new treatments are needed to improve the lives of these neuropsychiatric disorder patients. Now, clinical failure in the process of drug discovery for neurodegenerative diseases is a common occurrence. As the population continues to age, the incidence of these diseases will also increase. As a result, the need for improved treatments for neuropsychiatric disorders will follow. So, new drug discovery for these diseases remains a hot topic.

This Special Issue aims to provide a platform for original research papers, short communications, and review articles on latest advances in drug development for neurodegenerative diseases, and potentially showing additional disease-modifying properties to address neurodegeneration. These papers may cover multidisciplinary aspects (such as drug design, synthesis, and pharmacological evaluation) of novel drugs with potential therapeutic innovations.

Prof. Dr. Zhongzhen Zhou
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Molecules is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • drug discovery
  • neurodegenerative diseases
  • Alzheimer's disease
  • Parkinson's disease
  • depression
  • Huntington disease
  • amyotrophic lateral sclerosis
  • cerebral ischemia
  • cerebral injury
  • epilepsy

Published Papers (3 papers)

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Research

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37 pages, 4316 KiB  
Article
Effect of Natural Adenylcyclase/cAMP/CREB Signalling Activator Forskolin against Intra-Striatal 6-OHDA-Lesioned Parkinson’s Rats: Preventing Mitochondrial, Motor and Histopathological Defects
by Metab Alharbi, Abdulrahman Alshammari, Gurpreet Kaur, Sanjeev Kalra, Sidharth Mehan, Manisha Suri, Swesha Chhabra, Nitish Kumar, Wael A. Alanazi, Aliah R. Alshanwani, Abdullah Hamed AL-Ghamdi, Acharan S. Narula and Reni Kalfin
Molecules 2022, 27(22), 7951; https://doi.org/10.3390/molecules27227951 - 17 Nov 2022
Cited by 9 | Viewed by 2570
Abstract
Parkinson’s disease (PD) is characterised by dopaminergic neuronal loss in the brain area. PD is a complex disease that deteriorates patients’ motor and non-motor functions. In experimental animals, the neurotoxin 6-OHDA induces neuropathological, behavioural, neurochemical and mitochondrial abnormalities and the formation of free [...] Read more.
Parkinson’s disease (PD) is characterised by dopaminergic neuronal loss in the brain area. PD is a complex disease that deteriorates patients’ motor and non-motor functions. In experimental animals, the neurotoxin 6-OHDA induces neuropathological, behavioural, neurochemical and mitochondrial abnormalities and the formation of free radicals, which is related to Parkinson-like symptoms after inter-striatal 6-OHDA injection. Pathological manifestations of PD disrupt the cAMP/ATP-mediated activity of the transcription factor CREB, resulting in Parkinson’s-like symptoms. Forskolin (FSK) is a direct AC/cAMP/CREB activator isolated from Coleus forskohlii with various neuroprotective properties. FSK has already been proven in our laboratory to directly activate the enzyme adenylcyclase (AC) and reverse the neurodegeneration associated with the progression of Autism, Multiple Sclerosis, ALS, and Huntington’s disease. Several behavioural paradigms were used to confirm the post-lesion effects, including the rotarod, open field, grip strength, narrow beam walk (NBW) and Morris water maze (MWM) tasks. Our results were supported by examining brain cellular, molecular, mitochondrial and histopathological alterations. The FSK treatment (15, 30 and 45 mg/kg, orally) was found to be effective in restoring behavioural and neurochemical defects in a 6-OHDA-induced experimental rat model of PD. As a result, the current study successfully contributes to the investigation of FSK’s neuroprotective role in PD prevention via the activation of the AC/cAMP/PKA-driven CREB pathway and the restoration of mitochondrial ETC-complex enzymes. Full article
(This article belongs to the Special Issue Drug Development for Neurodegenerative Diseases)
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Review

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22 pages, 1105 KiB  
Review
Lipopolysaccharide-Induced Model of Neuroinflammation: Mechanisms of Action, Research Application and Future Directions for Its Use
by Anna Skrzypczak-Wiercioch and Kinga Sałat
Molecules 2022, 27(17), 5481; https://doi.org/10.3390/molecules27175481 - 26 Aug 2022
Cited by 55 | Viewed by 9141
Abstract
Despite advances in antimicrobial and anti-inflammatory therapies, inflammation and its consequences still remain a significant problem in medicine. Acute inflammatory responses are responsible for directly life-threating conditions such as septic shock; on the other hand, chronic inflammation can cause degeneration of body tissues [...] Read more.
Despite advances in antimicrobial and anti-inflammatory therapies, inflammation and its consequences still remain a significant problem in medicine. Acute inflammatory responses are responsible for directly life-threating conditions such as septic shock; on the other hand, chronic inflammation can cause degeneration of body tissues leading to severe impairment of their function. Neuroinflammation is defined as an inflammatory response in the central nervous system involving microglia, astrocytes, and cytokines including chemokines. It is considered an important cause of neurodegerative diseases, such as Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis. Lipopolysaccharide (LPS) is a strong immunogenic particle present in the outer membrane of Gram-negative bacteria. It is a major triggering factor for the inflammatory cascade in response to a Gram-negative bacteria infection. The use of LPS as a strong pro-inflammatory agent is a well-known model of inflammation applied in both in vivo and in vitro studies. This review offers a summary of the pathogenesis associated with LPS exposure, especially in the field of neuroinflammation. Moreover, we analyzed different in vivo LPS models utilized in the area of neuroscience. This paper presents recent knowledge and is focused on new insights in the LPS experimental model. Full article
(This article belongs to the Special Issue Drug Development for Neurodegenerative Diseases)
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18 pages, 1427 KiB  
Review
Neuroprotection of Cannabidiol, Its Synthetic Derivatives and Combination Preparations against Microglia-Mediated Neuroinflammation in Neurological Disorders
by Muhammad Yousaf, Dennis Chang, Yang Liu, Tianqing Liu and Xian Zhou
Molecules 2022, 27(15), 4961; https://doi.org/10.3390/molecules27154961 - 4 Aug 2022
Cited by 25 | Viewed by 6187
Abstract
The lack of effective treatment for neurological disorders has encouraged the search for novel therapeutic strategies. Remarkably, neuroinflammation provoked by the activated microglia is emerging as an important therapeutic target for neurological dysfunction in the central nervous system. In the pathological context, the [...] Read more.
The lack of effective treatment for neurological disorders has encouraged the search for novel therapeutic strategies. Remarkably, neuroinflammation provoked by the activated microglia is emerging as an important therapeutic target for neurological dysfunction in the central nervous system. In the pathological context, the hyperactivation of microglia leads to neuroinflammation through the release of neurotoxic molecules, such as reactive oxygen species, proteinases, proinflammatory cytokines and chemokines. Cannabidiol (CBD) is a major pharmacologically active phytocannabinoids derived from Cannabis sativa L. CBD has promising therapeutic effects based on mounting clinical and preclinical studies of neurological disorders, such as epilepsy, multiple sclerosis, ischemic brain injuries, neuropathic pain, schizophrenia and Alzheimer’s disease. A number of preclinical studies suggested that CBD exhibited potent inhibitory effects of neurotoxic molecules and inflammatory modulators, highlighting its remarkable therapeutic potential for the treatment of numerous neurological disorders. However, the molecular mechanisms of action underpinning CBD’s effects on neuroinflammation appear to be complex and are poorly understood. This review summarises the anti-neuroinflammatory activities of CBD against various neurological disorders with a particular focus on their main molecular mechanisms of action, which were related to the downregulation of NADPH oxidase-mediated ROS, TLR4-NFκB and IFN-β-JAK-STAT pathways. We also illustrate the pharmacological action of CBD’s derivatives focusing on their anti-neuroinflammatory and neuroprotective effects for neurological disorders. We included the studies that demonstrated synergistic enhanced anti-neuroinflammatory activity using CBD and other biomolecules. The studies that are summarised in the review shed light on the development of CBD, including its derivatives and combination preparations as novel therapeutic options for the prevention and/or treatment of neurological disorders where neuroinflammation plays an important role in the pathological components. Full article
(This article belongs to the Special Issue Drug Development for Neurodegenerative Diseases)
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