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Drug Design and Development for Neurological Diseases
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Drug Design and Development for Neurological Diseases

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

Deadline for manuscript submissions: 20 December 2024 | Viewed by 3510

Special Issue Editors

Prof. Dr. Alicja Nowaczyk

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Guest Editor
Department of Organic Chemistry, Faculty of Pharmacy, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University, 2 dr. A. Jurasza St., 85-094 Bydgoszcz, Poland
Interests: organic and medicinal chemistry; computational chemistry and molecular modeling of GAT, MAT, VGIC; predictive modelling of detailed mechanisms of action and pharmacological effec-tiveness of biologically active compounds and chemical reaction pathways; neuropharmacology; cardiovascular; safety pharmacology
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Grzegorz Grześk

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Guest Editor
Department of Cardiology and Clinical Pharmacology, Faculty of Health Sciences, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University, 75 Ujejskiego St., 85-168 Bydgoszcz, Poland
Interests: clinical and experimental pharmacology; cardiovascular pharmacology; internal medicine; en-dothelial function; vascular smooth muscle function; direct oral anticoagulants; therapeutic drug monitoring; antiplatelets agents
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurological disorders encompass a wide range of conditions that impact the neurological system, which comprises the brain, spinal cord and peripheral nerves. These disorders are intricate and frequently have a genetic basis. Manifestations of the condition can vary, including severe and prolonged discomfort, alterations in cognitive and behavioral patterns, as well as difficulties in motor functions. These illnesses can profoundly influence individuals, potentially resulting in life-threatening conditions and detrimentally impacting their quality of life.

Recent research has made notable progress in the advancement of medications for the treatment of neurological illnesses. Observing the efficacy of structure-based drug design and the therapeutic potential of nucleic acid-based therapeutics, such as plasmid DNA and NFκB decoy, in the treatment of neurological disorders is intriguing. Several writers have highlighted the significance of distinct strategies for aberrant protein folding and aggregation in neurodegenerative illnesses, while other researchers have concentrated on the utilization of polymeric nanoparticles for medication administration in these diseases. Research that specifically examines the process of repurposing existing medications for new uses in treating neurodegenerative illnesses is also deemed significant. These studies emphasize the diverse and promising approaches employed in the design and advancement of treatments for neurological disorders.

This Special Issue aims to bring together research on all aspects of molecular modeling in the neurotransmission phenomenon. It will contain high-quality research articles and review articles summarizing the state of the art in a specific area of this research field.

This Special Issue is supervised by Dr. Alicja Nowaczyk and assisted by our Topical Advisory Panel Member (Dr. Łukasz Fijałkowski, Nicolaus Copernicus University).

Prof. Dr. Alicja Nowaczyk
Prof. Dr. Grzegorz Grześk
Guest Editors

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • neurological disorders and their therapies
  • molecular modeling
  • synthesis and structural analysis
  • neurotransmitters ligands
  • mechanism of action
  • drug repurposing

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Published Papers (3 papers)

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Research

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19 pages, 4309 KiB  
Article
High-Salt Diet Accelerates Neuron Loss and Anxiety in APP/PS1 Mice Through Serpina3n
by Kaige Ma, Chenglin Zhang, Hanyue Zhang, Chanyuan An, Ge Li, Lixue Cheng, Mai Li, Minghe Ren, Yudan Bai, Zichang Liu, Shengfeng Ji, Xiyue Liu, Jinman Gao, Zhichao Zhang, Xiaolin Wu and Xinlin Chen
Int. J. Mol. Sci. 2024, 25(21), 11731; https://doi.org/10.3390/ijms252111731 - 31 Oct 2024
Viewed by 546
Abstract
High salt (HS) consumption is an independent risk factor for neurodegenerative diseases such as dementia, stroke, and cerebral small vessel disease related to cognitive decline. Recently, Alzheimer’s disease-like pathology changes have been reported as consequences of a HS diet in wild-type (wt) mice. [...] Read more.
High salt (HS) consumption is an independent risk factor for neurodegenerative diseases such as dementia, stroke, and cerebral small vessel disease related to cognitive decline. Recently, Alzheimer’s disease-like pathology changes have been reported as consequences of a HS diet in wild-type (wt) mice. However, it has not been revealed how HS diets accelerate the progress of Alzheimer’s disease (AD) in APP/PS1 mice. Here, we fed APP/PS1 mice a HS diet or normal diet (ND) for six months; the effects of the HS/ND on wt mice were also observed. The results of our behavior test reveal that the HS diet exacerbates anxiety, β-amyloid overload, neuron loss, and synapse damage in the hippocampi of APP/PS1 mice; this was not observed in HS-treated wt mice. RNA sequencing shows that nearly all serpin family members were increased in the hippocampus of HS-treated APP/PS1 mice. Gene function analysis showed that a HS diet induces neurodegeneration, including axon dysfunction and neuro-ligand-based dysfunction, and regulates serine protein inhibitor activities. The mRNA and protein levels of Serpina3n were dramatically increased. Upregulated Serpina3n may be the key for β-amyloid aggregation and neuronal loss in the hippocampus of HS-treated APP/PS1 mice. Serpina3n inhibition attenuated the anxiety and increased the number of neurons in the hippocampal CA1(cornu ammonis) region of APP/PS1 mice. Our study provides novel insights into the mechanisms by which excessive HS diet deteriorates anxiety in AD mice. Therefore, decreasing daily dietary salt consumption constitutes a pivotal public health intervention for mitigating the progression of neuropathology, especially for old patients and those with neurodegenerative disease. Full article
(This article belongs to the Special Issue Drug Design and Development for Neurological Diseases)
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16 pages, 1848 KiB  
Article
Effects of SRI-32743, a Novel Quinazoline Structure-Based Compound, on HIV-1 Tat and Cocaine Interaction with Norepinephrine Transporter
by Ana Catya Jiménez-Torres, Katherine D. Porter, Jamison A. Hastie, Charles Adeniran, Omar Moukha-Chafiq, Theresa H. Nguyen, Subramaniam Ananthan, Corinne E. Augelli-Szafran, Chang-Guo Zhan and Jun Zhu
Int. J. Mol. Sci. 2024, 25(14), 7881; https://doi.org/10.3390/ijms25147881 - 18 Jul 2024
Viewed by 827
Abstract
Prolonged exposure to HIV-1 transactivator of transcription (Tat) protein dysregulates monoamine transmission, a physiological change implicated as a key factor in promoting neurocognitive disorders among people living with HIV. We have demonstrated that in vivo expression of Tat in Tat transgenic mice decreases [...] Read more.
Prolonged exposure to HIV-1 transactivator of transcription (Tat) protein dysregulates monoamine transmission, a physiological change implicated as a key factor in promoting neurocognitive disorders among people living with HIV. We have demonstrated that in vivo expression of Tat in Tat transgenic mice decreases dopamine uptake through both dopamine transporter (DAT) and norepinephrine transporter (NET) in the prefrontal cortex. Further, our novel allosteric inhibitor of monoamine transporters, SRI-32743, has been shown to attenuate Tat-inhibited dopamine transport through DAT and alleviates Tat-potentiated cognitive impairments. The current study reports the pharmacological profiles of SRI-32743 in basal and Tat-induced inhibition of human NET (hNET) function. SRI-32743 exhibited less affinity for hNET binding than desipramine, a classical NET inhibitor, but displayed similar potency for inhibiting hDAT and hNET activity. SRI-32743 concentration-dependently increased hNET affinity for [3H]DA uptake but preserved the Vmax of dopamine transport. SRI-32743 slowed the cocaine-mediated dissociation of [3H]Nisoxetine binding and reduced both [3H]DA and [3H]MPP+ efflux but did not affect d-amphetamine-mediated [3H]DA release through hNET. Finally, we determined that SRI-32743 attenuated a recombinant Tat1–86-induced decrease in [3H]DA uptake via hNET. Our findings demonstrated that SRI-32743 allosterically disrupts the recombinant Tat1–86–hNET interaction, suggesting a potential treatment for HIV-infected individuals with concurrent cocaine abuse. Full article
(This article belongs to the Special Issue Drug Design and Development for Neurological Diseases)
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Review

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25 pages, 3805 KiB  
Review
Translational Relevance of Secondary Intracellular Signaling Cascades Following Traumatic Spinal Cord Injury
by Mohammad-Masoud Zavvarian, Akshat D. Modi, Sarah Sadat, James Hong and Michael G. Fehlings
Int. J. Mol. Sci. 2024, 25(11), 5708; https://doi.org/10.3390/ijms25115708 - 24 May 2024
Cited by 2 | Viewed by 1665
Abstract
Traumatic spinal cord injury (SCI) is a life-threatening and life-altering condition that results in debilitating sensorimotor and autonomic impairments. Despite significant advances in the clinical management of traumatic SCI, many patients continue to suffer due to a lack of effective therapies. The initial [...] Read more.
Traumatic spinal cord injury (SCI) is a life-threatening and life-altering condition that results in debilitating sensorimotor and autonomic impairments. Despite significant advances in the clinical management of traumatic SCI, many patients continue to suffer due to a lack of effective therapies. The initial mechanical injury to the spinal cord results in a series of secondary molecular processes and intracellular signaling cascades in immune, vascular, glial, and neuronal cell populations, which further damage the injured spinal cord. These intracellular cascades present promising translationally relevant targets for therapeutic intervention due to their high ubiquity and conservation across eukaryotic evolution. To date, many therapeutics have shown either direct or indirect involvement of these pathways in improving recovery after SCI. However, the complex, multifaceted, and heterogeneous nature of traumatic SCI requires better elucidation of the underlying secondary intracellular signaling cascades to minimize off-target effects and maximize effectiveness. Recent advances in transcriptional and molecular neuroscience provide a closer characterization of these pathways in the injured spinal cord. This narrative review article aims to survey the MAPK, PI3K-AKT-mTOR, Rho-ROCK, NF-κB, and JAK-STAT signaling cascades, in addition to providing a comprehensive overview of the involvement and therapeutic potential of these secondary intracellular pathways following traumatic SCI. Full article
(This article belongs to the Special Issue Drug Design and Development for Neurological Diseases)
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