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Biomolecular Approaches and Drugs for Neurodegeneration

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A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Chemical Biology".

Deadline for manuscript submissions: closed (30 November 2024) | Viewed by 31467

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Dr. Giovanni N. Roviello

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Institute of Biostructures and Bioimaging, Italian National Council for Research (IBB-CNR), Via P. Castellino 111, 80131 Naples, Italy
Interests: spectroscopy; computational chemistry; biomolecular binding; bioactive compounds; drug discovery
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Dr. Caterina Vicidomini

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Istituto di Biostrutture e Bioimmagini IBB-CNR, Via Tommaso De Amicis 95, 80145 Naples, Italy
Interests: pharmaceutical chemistry; neurodrugs; protein interactions; spectroscopy; computational chemistry; phytochemistry
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neuropathies are very common and disabling neuropathies affecting the ever-growing aged population around the world, especially in Western countries. There is an urgent need to develop effective therapies for preventing or treating neuropathies. Protein/peptide aggregation is of fundamental importance in therapeutics because this type of event is related to pathologies of enormous social relevance, including neurodegeneration. Interestingly, G-quadruplex (G4) DNA and RNA structures are also related to several neuropathies, and ligands able to destabilize or modulate the aggregation of such nucleic acid secondary structures are therefore envisaged to work as neurodrugs. In this Special Issue, we wish to focus on the more recent experimental and theoretical approaches for neurodrug design and development, with particular attention paid to the mechanisms of drug interference with protein and peptide aggregation pathways; however, contributions on G4 nucleic acid–drug interaction, G4 targets in neurodegenerative diseases, and nucleopeptide chemistry are also welcome, as they could improve the overall knowledge on the aggregation-based biochemistry at the interface between neurodrug design and therapy. Other themes of interest are inherent the computational chemistry and machine learning applied to chemistry and biology in the context of neuropathology therapy. This Special Issue is open to the submission of both original articles and reviews that describe research and ideas on themes treated in this Special Issue for neurodegeneration-related molecular strategies.

Dr. Giovanni N. Roviello
Dr. Caterina Vicidomini
Guest Editors

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Keywords

proteins
peptides
amyloid
Alzheimer disease
Parkinson’s disease
neurodrugs
G-quadruplex nucleic acids
biotechnology
biomolecular targets
peptide aggregation
natural products
synthetic drugs
antiamyloid therapeutics
machine learning

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Biomolecular Approaches and Drugs for Neurodegeneration—2nd Edition in Biomolecules (1 article)

Published Papers (11 papers)

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Research

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21 pages, 6147 KiB

Open AccessArticle

Multifaceted Role of Specialized Neuropeptide-Intensive Neurons on the Selective Vulnerability to Alzheimer’s Disease in the Human Brain

by Manci Li, Nicole Flack and Peter A. Larsen

Biomolecules 2024, 14(12), 1518; https://doi.org/10.3390/biom14121518 - 27 Nov 2024

Viewed by 991

Abstract

Regarding Alzheimer’s disease (AD), specific neuronal populations and brain regions exhibit selective vulnerability. Understanding the basis of this selective neuronal and regional vulnerability is essential to elucidate the molecular mechanisms underlying AD pathology. However, progress in this area is currently hindered by the incomplete understanding of the intricate functional and spatial diversity of neuronal subtypes in the human brain. Previous studies have demonstrated that neuronal subpopulations with high neuropeptide (NP) co-expression are disproportionately absent in the entorhinal cortex of AD brains at the single-cell level, and there is a significant decline in hippocampal NP expression in naturally aging human brains. Given the role of NPs in neuroprotection and the maintenance of microenvironments, we hypothesize that neurons expressing higher levels of NPs (HNP neurons) possess unique functional characteristics that predispose them to cellular abnormalities, which can manifest as degeneration in AD with aging. To test this hypothesis, multiscale and spatiotemporal transcriptome data from ~1900 human brain samples were analyzed using publicly available datasets. The results indicate that HNP neurons experienced greater metabolic burden and were more prone to protein misfolding. The observed decrease in neuronal abundance during stages associated with a higher risk of AD, coupled with the age-related decline in the expression of AD-associated neuropeptides (ADNPs), provides temporal evidence supporting the role of NPs in the progression of AD. Additionally, the localization of ADNP-producing HNP neurons in AD-associated brain regions provides neuroanatomical support for the concept that cellular/neuronal composition is a key factor in regional AD vulnerability. This study offers novel insights into the molecular and cellular basis of selective neuronal and regional vulnerability to AD in human brains. Full article

(This article belongs to the Special Issue Biomolecular Approaches and Drugs for Neurodegeneration)

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23 pages, 5375 KiB

Open AccessArticle

Inhibiting the Cholesterol Storage Enzyme ACAT1/SOAT1 in Myelin Debris-Treated Microglial Cell Lines Activates the Gene Expression of Cholesterol Efflux Transporter ABCA1

by Thao N. Huynh, Matthew C. Havrda, George J. Zanazzi, Catherine C. Y. Chang and Ta Yuan Chang

Biomolecules 2024, 14(10), 1301; https://doi.org/10.3390/biom14101301 - 14 Oct 2024

Cited by 1 | Viewed by 2389

Abstract

Aging is the major risk factor for Alzheimer’s disease (AD). In the aged brain, myelin debris accumulates and is cleared by microglia. Phagocytosed myelin debris increases neutral lipid droplet content in microglia. Neutral lipids include cholesteryl esters (CE) and triacylglycerol (TAG). To examine the effects of myelin debris on neutral lipid content in microglia, we added myelin debris to human HMC3 and mouse N9 cells. The results obtained when using ³H-oleate as a precursor in intact cells reveal that myelin debris significantly increases the biosynthesis of CE but not TAG. Mass analyses have shown that myelin debris increases both CE and TAG. The increase in CE biosynthesis was abolished using inhibitors of the cholesterol storage enzyme acyl-CoA:cholesterol acyltransferase 1 (ACAT1/SOAT1). ACAT1 inhibitors are promising drug candidates for AD treatment. In myelin debris-loaded microglia, treatment with two different ACAT1 inhibitors, K604 and F12511, increased the mRNA and protein content of ATP-binding cassette subfamily A1 (ABCA1), a protein that is located at the plasma membrane and which controls cellular cholesterol disposal. The effect of the ACAT1 inhibitor on ABCA1 was abolished by preincubating cells with the liver X receptor (LXR) antagonist GSK2033. We conclude that ACAT1 inhibitors prevent the accumulation of cholesterol and CE in myelin debris-treated microglia by activating ABCA1 gene expression via the LXR pathway. Full article

(This article belongs to the Special Issue Biomolecular Approaches and Drugs for Neurodegeneration)

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10 pages, 2331 KiB

Open AccessArticle

Screening of Anti-Prion Compounds Using the Protein Misfolding Cyclic Amplification Technology

by Sandra Pritzkow, Isaac Schauer, Ananya Tupaki-Sreepurna, Rodrigo Morales and Claudio Soto

Biomolecules 2024, 14(9), 1113; https://doi.org/10.3390/biom14091113 - 4 Sep 2024

Viewed by 1632

Abstract

Prion diseases are 100% fatal infectious neurodegenerative diseases affecting the brains of humans and other mammals. The disease is caused by the formation and replication of prions, composed exclusively of the misfolded prion protein (PrP^Sc). We invented and developed the protein misfolding cyclic amplification (PMCA) technology for in vitro prion replication, which allow us to replicate the infectious agent and it is commonly used for ultra-sensitive prion detection in biological fluids, tissues and environmental samples. In this article, we studied whether PMCA can be used to screen for chemical compounds that block prion replication. A small set of compounds previously shown to have anti-prion activity in various systems, mostly using cells infected with murine prions, was evaluated for their ability to prevent the replication of prions. Studies were conducted simultaneously with prions derived from 4 species, including human, cattle, cervid and mouse. Our results show that only one of these compounds (methylene blue) was able to completely inhibit prion replication in all species. Estimation of the IC50 for methylene blue inhibition of human prions causing variant Creutzfeldt-Jakob disease (vCJD) was 7.7 μM. Finally, we showed that PMCA can be used for structure-activity relationship studies of anti-prion compounds. Interestingly, some of the less efficient prion inhibitors altered the replication of prions in some species and not others, suggesting that PMCA is useful for studying the differential selectivity of potential drugs. Full article

(This article belongs to the Special Issue Biomolecular Approaches and Drugs for Neurodegeneration)

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20 pages, 2583 KiB

Open AccessEditor’s ChoiceArticle

A High-Throughput Screening of a Natural Products Library for Mitochondria Modulators

by Emmanuel Makinde, Linlin Ma, George D. Mellick and Yunjiang Feng

Biomolecules 2024, 14(4), 440; https://doi.org/10.3390/biom14040440 - 4 Apr 2024

Cited by 2 | Viewed by 2036

Abstract

Mitochondria, the energy hubs of the cell, are progressively becoming attractive targets in the search for potent therapeutics against neurodegenerative diseases. The pivotal role of mitochondrial dysfunction in the pathogenesis of various diseases, including Parkinson’s disease (PD), underscores the urgency of discovering novel therapeutic strategies. Given the limitations associated with available treatments for mitochondrial dysfunction-associated diseases, the search for new potent alternatives has become imperative. In this report, we embarked on an extensive screening of 4224 fractions from 384 Australian marine organisms and plant samples to identify natural products with protective effects on mitochondria. Our initial screening using PD patient-sourced olfactory neurosphere-derived (hONS) cells with rotenone as a mitochondria stressor resulted in 108 promising fractions from 11 different biota. To further assess the potency and efficacy of these hits, the 11 biotas were subjected to a subsequent round of screening on human neuroblastoma (SH-SY5Y) cells, using 6-hydroxydopamine to induce mitochondrial stress, complemented by a mitochondrial membrane potential assay. This rigorous process yielded 35 active fractions from eight biotas. Advanced analysis using an orbit trap mass spectrophotometer facilitated the identification of the molecular constituents of the most active fraction from each of the eight biotas. This meticulous approach led to the discovery of 57 unique compounds, among which 12 were previously recognized for their mitoprotective effects. Our findings highlight the vast potential of natural products derived from Australian marine organisms and plants in the quest for innovative treatments targeting mitochondrial dysfunction in neurodegenerative diseases. Full article

(This article belongs to the Special Issue Biomolecular Approaches and Drugs for Neurodegeneration)

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18 pages, 6004 KiB

Open AccessEditor’s ChoiceArticle

Neuroprotective Effects of the Nutraceutical Dehydrozingerone and Its C₂-Symmetric Dimer in a Drosophila Model of Parkinson’s Disease

by Maria Dolores Setzu, Ignazia Mocci, Davide Fabbri, Paola Carta, Patrizia Muroni, Andrea Diana, Maria Antonietta Dettori and Maria Antonietta Casu

Biomolecules 2024, 14(3), 273; https://doi.org/10.3390/biom14030273 - 24 Feb 2024

Viewed by 3114

Abstract

Parkinson’s disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons responsible for unintended or uncontrollable movements. Mutations in the leucine-rich repeat kinase 2 locus contribute to genetic forms of PD. The fruit fly Drosophila melanogaster carrying this mutation (LRRK2-Dm) is an in vivo model of PD that develops motor impairment and stands for an eligible non-mammalian paradigm to test novel therapeutic approaches. Dehydrozingerone (DHZ) is a natural phenolic compound isolated from ginger and presents anti-inflammatory, antioxidant and neuroprotective properties, making it a potential therapeutic target for PD. We administered DHZ and its C₂-symmetric dimer (DHZ-DIM) at 0.5 and 1 mM for 14 and 21 days in the LRRK2-Dm, with the aim of assessing changes in rescuing motor behavior, brain dopaminergic neurons, mitochondria and synapses (T-bars). The shorter treatment with both molecules revealed efficacy at the higher dose, improving climbing behavior with a prevention of dopaminergic neuronal demise. After 21 days, a recovery of the motor disability, dopaminergic neuron loss, mitochondrial damage and T-bars failure was observed with the DHZ-DIM. Our data indicate that the DHZ-DIM exerts a more potent neuroprotective effect with respect to the monomer in LRRK2-Dm, prompting further investigation of these compounds in rodent models of PD. Full article

(This article belongs to the Special Issue Biomolecular Approaches and Drugs for Neurodegeneration)

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13 pages, 2604 KiB

Open AccessEditor’s ChoiceArticle

Ladostigil Reduces the Adenoside Triphosphate/Lipopolysaccharide-Induced Secretion of Pro-Inflammatory Cytokines from Microglia and Modulate-Immune Regulators, TNFAIP3, and EGR1

by Fanny Reichert, Keren Zohar, Elyad Lezmi, Tsiona Eliyahu, Shlomo Rotshenker, Michal Linial and Marta Weinstock

Biomolecules 2024, 14(1), 112; https://doi.org/10.3390/biom14010112 - 16 Jan 2024

Cited by 4 | Viewed by 2277

Abstract

Treatment of aging rats for 6 months with ladostigil (1 mg/kg/day) prevented a decline in recognition and spatial memory and suppressed the overexpression of gene-encoding pro-inflammatory cytokines, TNFα, IL1β, and IL6 in the brain and microglial cultures. Primary cultures of mouse microglia stimulated by lipopolysaccharides (LPS, 0.75 µg/mL) and benzoyl ATPs (BzATP) were used to determine the concentration of ladostigil that reduces the secretion of these cytokine proteins. Ladostigil (1 × 10⁻¹¹ M), a concentration compatible with the blood of aging rats in, prevented memory decline and reduced secretion of IL1β and IL6 by ≈50%. RNA sequencing analysis showed that BzATP/LPS upregulated 25 genes, including early-growth response protein 1, (Egr1) which increased in the brain of subjects with neurodegenerative diseases. Ladostigil significantly decreased Egr1 gene expression and levels of the protein in the nucleus and increased TNF alpha-induced protein 3 (TNFaIP3), which suppresses cytokine release, in the microglial cytoplasm. Restoration of the aberrant signaling of these proteins in ATP/LPS-activated microglia in vivo might explain the prevention by ladostigil of the morphological and inflammatory changes in the brain of aging rats. Full article

(This article belongs to the Special Issue Biomolecular Approaches and Drugs for Neurodegeneration)

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Review

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23 pages, 1038 KiB

Open AccessReview

Neuroprotective Properties of Clove (Syzygium aromaticum): State of the Art and Future Pharmaceutical Applications for Alzheimer’s Disease

by Tatevik Sargsyan, Hayarpi M. Simonyan, Lala Stepanyan, Avetis Tsaturyan, Caterina Vicidomini, Raffaele Pastore, Germano Guerra and Giovanni N. Roviello

Biomolecules 2025, 15(3), 452; https://doi.org/10.3390/biom15030452 - 20 Mar 2025

Viewed by 1864

Abstract

This study explores the neuropharmacological potential of various molecular and amino acid components derived from Syzygium aromaticum (clove), an aromatic spice with a long history of culinary and medicinal use. Key bioactive compounds such as eugenol, α-humulene, β-caryophyllene, gallic acid, quercetin, and luteolin demonstrate antioxidant, anti-inflammatory, and neuroprotective properties by scavenging free radicals, modulating calcium channels, and reducing neuroinflammation and oxidative stress. Moreover, gallic acid and asiatic acid may exhibit protective effects, including neuronal apoptosis inhibition, while other useful properties of clove phytocompounds include NF-κB pathway inhibition, membrane stabilization, and suppression of pro-inflammatory pathways, possibly in neurons or other relevant cell types, further contributing to neuroprotection and cognitive enhancement. Amino acid analysis revealed essential and non-essential amino acids such as aspartic acid, serine, glutamic acid, glycine, histidine, and arginine in various clove parts (buds, fruits, branches, and leaves). These amino acids play crucial roles in neurotransmitter synthesis, immune modulation, antioxidant defense, and metabolic regulation. Collectively, these bioactive molecules and amino acids contribute to clove’s antioxidant, anti-inflammatory, neurotrophic, and neurotransmitter-modulating effects, highlighting its potential as a preventive and therapeutic candidate for neurodegenerative disorders. While preliminary preclinical studies support these neuroprotective properties, further research, including clinical trials, is needed to validate the efficacy and safety of clove-based interventions in neuroprotection. Full article

(This article belongs to the Special Issue Biomolecular Approaches and Drugs for Neurodegeneration)

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20 pages, 713 KiB

Open AccessReview

Deciphering the Role of Adrenergic Receptors in Alzheimer’s Disease: Paving the Way for Innovative Therapies

by Androulla N. Miliotou, Andria Kotsoni and Lefteris C. Zacharia

Biomolecules 2025, 15(1), 128; https://doi.org/10.3390/biom15010128 - 15 Jan 2025

Viewed by 4668

Abstract

Neurodegenerative diseases are currently among the most devastating diseases with no effective disease-modifying drugs in the market, with Alzheimer’s disease (AD) being the most prevalent. AD is a complex multifactorial neurodegenerative disorder characterized by progressive and severe cognitive impairment and memory loss. It is the most common cause of progressive memory loss (dementia) in the elderly, and to date, there is no effective treatment to cure or slow disease progression substantially. The role of adrenergic receptors in the pathogenesis of Alzheimer’s disease and other tauopathies is poorly understood or investigated. Recently, some studies indicated a potential benefit of drugs acting on the adrenergic receptors for AD and dementias, although due to the heterogeneity of the drug classes used, the results on the whole remain inconclusive. The scope of this review article is to comprehensively review the literature on the possible role of adrenergic receptors in neurodegenerative diseases, stemming from the use of agonists and antagonists including antihypertensive and asthma drugs acting on the adrenergic receptors, but also from animal models and in vitro models where these receptors have been studied. Ultimately, we hope to obtain a better understanding of the role of these receptors, identify the gaps in knowledge, and explore the possibility of repurposing such drugs for AD, given their long history of use and safety. Full article

(This article belongs to the Special Issue Biomolecular Approaches and Drugs for Neurodegeneration)

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13 pages, 774 KiB

Open AccessReview

Immunoglobulin G and Complement as Major Players in the Neurodegeneration of Multiple Sclerosis

by Peter G. E. Kennedy, Matthew Fultz, Jeremiah Phares and Xiaoli Yu

Biomolecules 2024, 14(10), 1210; https://doi.org/10.3390/biom14101210 - 26 Sep 2024

Cited by 1 | Viewed by 2051

Abstract

Multiple Sclerosis (MS) is an inflammatory, demyelinating, and neurodegenerative disease of the central nervous system (CNS) and is termed as one of the most common causes of neurological disability in young adults. Axonal loss and neuronal cell damage are the primary causes of disease progression and disability. Yet, little is known about the mechanism of neurodegeneration in the disease, a limitation that impairs the development of more effective treatments for progressive MS. MS is characterized by the presence of oligoclonal bands and raised levels of immunoglobulins in the CNS. The role of complement in the demyelinating process has been detected in both experimental animal models of MS and within the CNS of affected MS patients. Furthermore, both IgG antibodies and complement activation can be detected in the demyelinating plaques and cortical gray matter lesions. We propose here that both immunoglobulins and complement play an active role in the neurodegenerative process of MS. We hypothesize that the increased CNS IgG antibodies form IgG aggregates and bind complement C1q with high affinity, activating the classical complement pathway. This results in neuronal cell damage, which leads to neurodegeneration and demyelination in MS. Full article

(This article belongs to the Special Issue Biomolecular Approaches and Drugs for Neurodegeneration)

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29 pages, 2633 KiB

Open AccessEditor’s ChoiceReview

Therapeutic Strategies for Spinocerebellar Ataxia Type 1

by Laurie M. C. Kerkhof, Bart P. C. van de Warrenburg, Willeke M. C. van Roon-Mom and Ronald A. M. Buijsen

Biomolecules 2023, 13(5), 788; https://doi.org/10.3390/biom13050788 - 2 May 2023

Cited by 3 | Viewed by 7090

Abstract

Spinocerebellar ataxia type 1 (SCA1) is an autosomal dominant neurodegenerative disorder that affects one or two individuals per 100,000. The disease is caused by an extended CAG repeat in exon 8 of the ATXN1 gene and is characterized mostly by a profound loss of cerebellar Purkinje cells, leading to disturbances in coordination, balance, and gait. At present, no curative treatment is available for SCA1. However, increasing knowledge on the cellular and molecular mechanisms of SCA1 has led the way towards several therapeutic strategies that can potentially slow disease progression. SCA1 therapeutics can be classified as genetic, pharmacological, and cell replacement therapies. These different therapeutic strategies target either the (mutant) ATXN1 RNA or the ataxin-1 protein, pathways that play an important role in downstream SCA1 disease mechanisms or which help restore cells that are lost due to SCA1 pathology. In this review, we will provide a summary of the different therapeutic strategies that are currently being investigated for SCA1. Full article

(This article belongs to the Special Issue Biomolecular Approaches and Drugs for Neurodegeneration)

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Other

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14 pages, 2979 KiB

Open AccessSystematic Review

A Systematic Review on Dementia and Translocator Protein (TSPO): When Nuclear Medicine Highlights an Underlying Expression

by Miriam Conte, Maria Silvia De Feo, Ferdinando Corica, Joana Gorica, Marko Magdi Abdou Sidrak, Flaminia De Cristofaro, Luca Filippi, Maria Ricci, Giuseppe De Vincentis and Viviana Frantellizzi

Biomolecules 2023, 13(4), 598; https://doi.org/10.3390/biom13040598 - 26 Mar 2023

Viewed by 2021

Abstract

Background: Translocator protein (TSPO) is a neuroinflammation hallmark. Different TSPO affinity compounds have been produced and over time, the techniques of radiolabeling have been refined. The aim of this systematic review is to summarize the development of new radiotracers for dementia and neuroinflammation imaging. Methods: An online search of the literature was conducted in the PubMed, Scopus, Medline, Cochrane Library, and Web of Science databases, selecting published studies from January 2004 to December 2022. The accepted studies considered the synthesis of TSPO tracers for nuclear medicine imaging in dementia and neuroinflammation. Results: A total of 50 articles was identified. Twelve papers were selected from the included studies’ bibliographies and 34 were excluded. Thus, 28 articles were ultimately selected for quality assessment. Conclusion: Huge efforts in developing specific and stable tracers for PET/SPECT imaging have been made. The long half-life of ¹⁸F makes this isotope a preferable choice to ¹¹C. An emerging limitation to this however is that neuroinflammation involves all of the brain which inhibits the possibility of detecting a slight inflammation status change in patients. A partial solution to this is using the cerebellum as a reference region and developing higher TSPO affinity tracers. Moreover, it is necessary to consider the presence of distomers and racemic compounds interfering with pharmacological tracers’ effects and increasing the noise ratio in images. Full article

(This article belongs to the Special Issue Biomolecular Approaches and Drugs for Neurodegeneration)

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