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Mechanisms and Interventions for Neurological and Psychological Disorders

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

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 32676

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Dr. Majid Davidson

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Institute for Health and Sport, Victoria University, Melbourne, VIC 3021, Australia
Interests: nanoparticles; vaccines; depression; neuroimmunology; gut-brain axis; neuropsychiatric disorders
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Vasso Apostolopoulos

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Institute for Health and Sport, Victoria University, Melbourne, VIC 3011, Australia
Interests: immunology; protein crystallography; medicinal chemistry; cellular and molecular biology; extensive translational research; clinical trials; vaccines; drugs; healthy ageing; chronic diseases; inflammation
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Prof. Dr. Tissa Wijeratne

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AIMSS, Department of Neurology, Melbourne Medical School, Sunshine Hospital, Western Health, The University of Melbourne, Melbourne, VIC 3011, Australia
Interests: migraine; brain injury; stroke; neurology; headache
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues

Neurological conditions affect the brain, the spinal cord, and nerves found throughout the body. There are over 600 neurological conditions that affect humans, some of which include, dementia, epilepsy, multiple sclerosis, motor neuron disease, and headache (see keywords for other neurological disorder examples). Abnormalities in the brain, spinal cord or nerves including structural, biochemical or electrical leads to symptoms of a neurological condition. Some symptoms include muscle weakness, loss of coordination and sensation, seizures, paralysis, etc. The causes of neurological disorders vary but can be due to infections, tumors, environmental, lifestyle, genetic, congenital, trauma.

There is also a vast range of psychological disorders some of which include, bipolar, eating disorders, paranoia, psychosis, schizophrenia, social anxiety disorder, phobias, agoraphobia, panic attacks and neuropsychiatric disorders. These disorders can be genetic, biological, chemical imbalance in the brain, traumatic brain injury, history of abuse, stress, viral, chemical, cancer, alcohol, or recreational substance abuse drugs.

This Special Issue aims to collect contributions related to mechanisms of disease including at the molecular, cellular, genetic, biochemical and immunological levels. We also seek articles on interventions used to manage these diorders.

You are invited to submit original experimental research papers, theoretical papers, reviews, systematic reviews, meta-analyses, communications, reports, and notes. We look forward to your valuable contributions.

Dr. Majid Davidson
Prof. Dr. Vasso Apostolopoulos
Prof. Dr. Tissa Wijeratne
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

cerebral palsy
headaches
stroke
Bell’s palsy
neurodegeneration
dementia
Parkinson’s disease
Alzheimer’s disease
Huntington’s disease
Guillain–Barre syndrome
multiple sclerosis
brain cancer
myasthenia gravis
neuromuscular disorders
muscular dystrophy
amyotrophic lateral sclerosis
motor neuron disease
neurodevelopment disorders
learning disabilities
autism
mental retardation
attention deficit disorder
ataxia
epilepsy, seizures
gut-brain axis
traumatic brain injury
Tourette syndrome
shingles
meningitis
encephalitis
psychological disorder
bipolar
eating disorders
paranoia
psychosis
schizophrenia
neuropsychiatric disorder
depression, anxiety
ageing
virus infections
cancer
molecular
cellular
immunological aspects
genetic
interventions
mechanisms

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Published Papers (11 papers)

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Research

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18 pages, 6304 KiB

Open AccessArticle

Development of p-Tau Differentiated Cell Model of Alzheimer’s Disease to Screen Novel Acetylcholinesterase Inhibitors

by Giuseppe Uras, Xinuo Li, Alessia Manca, Antonella Pantaleo, Marco Bo, Jinyi Xu, Stephanie Allen and Zheying Zhu

Int. J. Mol. Sci. 2022, 23(23), 14794; https://doi.org/10.3390/ijms232314794 - 26 Nov 2022

Cited by 1 | Viewed by 1559

Abstract

Alzheimer’s disease (AD) is characterized by an initial accumulation of amyloid plaques and neurofibrillary tangles, along with the depletion of cholinergic markers. The currently available therapies for AD do not present any disease-modifying effects, with the available in vitro platforms to study either AD drug candidates or basic biology not fully recapitulating the main features of the disease or being extremely costly, such as iPSC-derived neurons. In the present work, we developed and validated a novel cell-based AD model featuring Tau hyperphosphorylation and degenerative neuronal morphology. Using the model, we evaluated the efficacy of three different groups of newly synthesized acetylcholinesterase (AChE) inhibitors, along with a new dual acetylcholinesterase/glycogen synthase kinase 3 inhibitor, as potential AD treatment on differentiated SH-SY5Y cells treated with glyceraldehyde to induce Tau hyperphosphorylation, and subsequently neurite degeneration and cell death. Testing of such compounds on the newly developed model revealed an overall improvement of the induced defects by inhibition of AChE alone, showing a reduction of S396 aberrant phosphorylation along with a moderate amelioration of the neuron-like morphology. Finally, simultaneous AChE/GSK3 inhibition further enhanced the limited effects observed by AChE inhibition alone, resulting in an improvement of all the key parameters, such as cell viability, morphology, and Tau abnormal phosphorylation. Full article

(This article belongs to the Special Issue Mechanisms and Interventions for Neurological and Psychological Disorders)

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13 pages, 2415 KiB

Open AccessArticle

SWATH Mass Spectrometry-Based CSF Proteome Profile of GBA-Linked Parkinson’s Disease Patients

by Saima Zafar, Aneeqa Noor, Neelam Younas, Mohsin Shafiq, Matthias Schmitz, Isabel Wurster, Kathrin Brockmann, Thomas Gasser and Inga Zerr

Int. J. Mol. Sci. 2022, 23(22), 14166; https://doi.org/10.3390/ijms232214166 - 16 Nov 2022

Cited by 2 | Viewed by 1500

Abstract

β-glucocerebrosidase (GBA)-associated mutations are a significant risk factor for Parkinson’s disease (PD) that aggravate the disease pathology by upregulating the deposition of α-Synuclein (α-Syn). The resultant clinical profile varies for PD patients without GBA mutations. The current study aimed to identify the proteomic targets involved in the pathogenic pathways leading to the differential clinical presentation of GBA-associated PD. CSF samples (n = 32) were obtained from PD patients with GBA mutations (n = 22), PD patients without GBA mutations (n = 7), and healthy controls that were carriers of GBA mutations (n = 3). All samples were subjected to in-gel tryptic digestion followed by the construction of the spectral library and quantitative SWATH-based analysis. CSF α-Syn levels were reduced in both PD_Idiopathic and PD_GBA cases. Our SWATH-based mass spectrometric analysis detected 363 proteins involved in immune response, stress response, and cell signaling in various groups. Intergroup analysis showed that 52 proteins were significantly up- or downregulated in various groups. Of these 52 targets, 20 proteins were significantly altered in PD_GBA cases only while 2 showed different levels in PD_Idiopathic patients. Our results show that the levels of several pathologically relevant proteins, including Contactin-1, Selenium-binding protein 1, Adhesion G Protein-Coupled Receptor, and Apolipoprotein E are significantly different among the sporadic and genetic variants of PD and hint at aggravated synaptic damage, oxidative stress, neuronal loss, and aggregation of α-Syn in PD_GBA cases. Full article

(This article belongs to the Special Issue Mechanisms and Interventions for Neurological and Psychological Disorders)

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10 pages, 1887 KiB

Open AccessArticle

Oxygenated Water Increases Seizure Threshold in Various Rodent Seizure Models

by Hyeok Hee Kwon, Seung Yeon Jung, Hyewon Park, Hyo Jung Shin, Dong Woon Kim, Hee-Jung Song and Joon Won Kang

Int. J. Mol. Sci. 2022, 23(22), 14124; https://doi.org/10.3390/ijms232214124 - 16 Nov 2022

Cited by 1 | Viewed by 1214

Abstract

Oxygenated water (OW) contains more oxygen than normal drinking water. It may induce oxygen enrichment in the blood and reduce oxidative stress. Hypoxia and oxidative stress could be involved in epilepsy. We aimed to examine the effects of OW-treated vs. control on four rodent models of epilepsy: (1) prenatal betamethasone priming with postnatal N-methyl-D-aspartate (NMDA)-triggered spasm, (2) no prenatal betamethasone, (3) repetitive kainate injection, and (4) intraperitoneal pilocarpine. We evaluated, in (1) and (2), the latency to onset and the total number of spasms; (3) the number of kainate injections required to induce epileptic seizures; (4) spontaneous recurrent seizures (SRS) (numbers and duration). In model (1), the OW-treated group showed significantly increased latency to onset and a decreased total number of spasms; in (2), OW completely inhibited spasms; in (3), the OW-treated group showed a significantly decreased number of injections required to induce epileptic seizures; and in (4), in the OW-treated group, the duration of a single SRS was significantly reduced. In summary, OW may increase the seizure threshold. Although the underlying mechanism remains unclear, OW may provide an adjunctive alternative for patients with refractory epilepsy. Full article

(This article belongs to the Special Issue Mechanisms and Interventions for Neurological and Psychological Disorders)

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14 pages, 3847 KiB

Open AccessArticle

Localization of the Neuropeptide Arginine Vasotocin and Its Receptor in the Osmoregulatory Organs of Black Porgy, Acanthopagrus schlegelii: Gills, Kidneys, and Intestines

by Ganesan Nagarajan, Aruna Adimoolam, Yousef Ahmed Alkhamis, Roshmon Thomas Mathew and Ching-Fong Chang

Int. J. Mol. Sci. 2022, 23(21), 13421; https://doi.org/10.3390/ijms232113421 - 03 Nov 2022

Cited by 1 | Viewed by 1214

Abstract

The neurohypophysial hormone arginine vasotocin (avt) and its receptor (avtr) regulates ions in the osmoregulatory organs of euryhaline black porgy (Acanthopagrus schlegelii). The localization of avt and avtr transcripts in the osmoregulatory organs has yet to be demonstrated. Thus, in the present study, we performed an in situ hybridization analysis to determine the localization of avt and avtr in the gills, kidneys, and intestines of the black porgy. The avt and avtr transcripts were identified in the filament and lamellae region of the gills in the black porgy. However, the basal membrane of the filament contained more avt and avtr transcripts. Fluorescence double tagging analysis revealed that avt and avtr mRNAs were partially co-localized with α-Nka-ir cells in the gill filament. The proximal tubules, distal tubules, and collecting duct of the kidney all had positive hybridization signals for the avt and avtr transcripts. Unlike the α-Nka immunoreactive cells, the avt and avtr transcripts were found on the basolateral surface of the distal convoluted tubule and in the entire cells of the proximal convoluted tubules of the black porgy kidney. In the intestine, the avt and avtr transcripts were found in the basolateral membrane of the enterocytes. Collectively, this study provides a summary of evidence suggesting that the neuropeptides avt and avtr with α-Nka-ir cells may have functions in the gills, kidneys, and intestines via ionocytes. Full article

(This article belongs to the Special Issue Mechanisms and Interventions for Neurological and Psychological Disorders)

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12 pages, 1978 KiB

Open AccessArticle

A Role of DNA Methylation within the CYP17A1 Gene in the Association of Genetic and Environmental Risk Factors with Stress-Related Manifestations of Schizophrenia

by Margarita Alfimova, Nikolay Kondratyev, Galina Korovaitseva, Tatyana Lezheiko, Victoria Plakunova, Marina Gabaeva and Vera Golimbet

Int. J. Mol. Sci. 2022, 23(20), 12629; https://doi.org/10.3390/ijms232012629 - 20 Oct 2022

Viewed by 1375

Abstract

As genetic and environmental influences on schizophrenia might converge on DNA methylation (DNAm) within loci which are both associated with the disease and implicated in response to environmental stress, we examined whether DNAm within CYP17A1, a hypothalamus–pituitary–adrenal axis gene which is situated within the schizophrenia risk locus 10q24.32, would mediate genetic and environmental effects on stress-related schizophrenia symptoms. DNAm within an exonic–intronic fragment of CYP17A1 was assessed in the blood of 66 schizophrenia patients and 63 controls using single-molecule real-time bisulfite sequencing. Additionally, the VNTR polymorphism of the AS3MT gene, a plausible causal variant within the 10q24.32 locus, was genotyped in extended patient and control samples (n = 700). The effects of local haplotype, VNTR and a polyenviromic risk score (PERS) on DNAm, episodic verbal memory, executive functions, depression, and suicidality of patients were assessed. Haplotype and PERS differentially influenced DNAm at four variably methylated sites identified within the fragment, with stochastic, additive, and allele-specific effects being found. An allele-specific DNAm at CpG-SNP rs3781286 mediated the relationship between the local haplotype and verbal fluency. Our findings do not confirm that the interrogated DNA fragment is a place where genetic and environmental risk factors converge to influence schizophrenia symptoms through DNAm. Full article

(This article belongs to the Special Issue Mechanisms and Interventions for Neurological and Psychological Disorders)

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11 pages, 627 KiB

Open AccessArticle

Aggression in Women with Schizophrenia Is Associated with Lower HDL Cholesterol Levels

by Dora Herceg, Ninoslav Mimica, Miroslav Herceg and Krešimir Puljić

Int. J. Mol. Sci. 2022, 23(19), 11858; https://doi.org/10.3390/ijms231911858 - 06 Oct 2022

Cited by 2 | Viewed by 1668

Abstract

This study assessed the association between serum lipid levels and aggression in female patients with schizophrenia. The study included female patients with schizophrenia (N = 120). The participants were subdivided into two groups (aggressive and nonaggressive), with 60 participants in each group. Serum lipids—cholesterol, triglycerides, high-density lipoproteins (HDL cholesterol), and low-density lipoproteins (LDL cholesterol)—were determined. The clinical part of the study included an evaluation using psychiatric scales: the positive and negative syndrome scale (PANSS), the aggression subscale of the PANSS scale (PANSS-AG), and the overt aggression scale (OAS). Significant differences were only observed in HDL cholesterol levels, where aggressive subjects had significantly lower values of HDL cholesterol (t = 2.540; p = 0.012), and the representation of subjects with low cholesterol values was almost three-times higher in the group of subjects with aggression (χ² = 7.007; p = 0.008) compared to the nonaggressive group. The nominally significant predictor for HDL cholesterol in nonaggressive and aggressive participants was the total value of the PANSS scores. In subjects with aggression, suicidality was not significantly associated with HDL cholesterol levels. Our findings suggest that lower HDL cholesterol is significantly associated with aggression in women with schizophrenia. Full article

(This article belongs to the Special Issue Mechanisms and Interventions for Neurological and Psychological Disorders)

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Review

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12 pages, 2233 KiB

Open AccessReview

Exercise-Induced Fibroblast Growth Factor-21: A Systematic Review and Meta-Analysis

by Hyunjoong Kim, Jihye Jung, Sungeon Park, Younglan Joo, Sangbong Lee, Jeongu Sim, Jinhyeong Choi, Hyun Lee, Gyujeong Hwang and Seungwon Lee

Int. J. Mol. Sci. 2023, 24(8), 7284; https://doi.org/10.3390/ijms24087284 - 14 Apr 2023

Cited by 3 | Viewed by 1794

Abstract

This systematic review aimed to synthesize and quantify the results of the studies investigating the changes in fibroblast growth factor-21 (FGF-21) induced by exercise. We searched for studies that did not differentiate between patients and healthy adults but compared them before and after exercise and with and without exercise. For quality assessment, the risk-of-bias assessment tool for nonrandomized studies and the Cochrane risk-of-bias tool were used. A quantitative analysis was performed using the standardized mean difference (SMD) and random-effects model in RevMan 5.4. A total of 94 studies were searched in international electronic databases, and after screening, 10 studies with 376 participants were analyzed. Compared with no exercise, there was a significant increase in the FGF-21 levels from before to after exercise (SMD = 1.05, 95% confidence interval (CI), 0.21 to 1.89). The changes in FGF-21 levels in the exercise group showed a significant difference from the levels in the controls. The results of the random-effects model were as follows: SMD = 1.12; 95% CI, −0.13 to 2.37. While the data on acute exercise were not synthesized in this study, FGF-21 levels generally increased after chronic exercise compared with no exercise. Full article

(This article belongs to the Special Issue Mechanisms and Interventions for Neurological and Psychological Disorders)

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16 pages, 586 KiB

Open AccessReview

Transient Receptor Potential (TRP) Channels in Pain, Neuropsychiatric Disorders, and Epilepsy

by Felix Yang, Andy Sivils, Victoria Cegielski, Som Singh and Xiang-Ping Chu

Int. J. Mol. Sci. 2023, 24(5), 4714; https://doi.org/10.3390/ijms24054714 - 01 Mar 2023

Cited by 6 | Viewed by 3091

Abstract

Pharmacomodulation of membrane channels is an essential topic in the study of physiological conditions and disease status. Transient receptor potential (TRP) channels are one such family of nonselective cation channels that have an important influence. In mammals, TRP channels consist of seven subfamilies with a total of twenty-eight members. Evidence shows that TRP channels mediate cation transduction in neuronal signaling, but the full implication and potential therapeutic applications of this are not entirely clear. In this review, we aim to highlight several TRP channels which have been shown to mediate pain sensation, neuropsychiatric disorders, and epilepsy. Recent findings suggest that TRPM (melastatin), TRPV (vanilloid), and TRPC (canonical) are of particular relevance to these phenomena. The research reviewed in this paper validates these TRP channels as potential targets of future clinical treatment and offers patients hope for more effective care. Full article

(This article belongs to the Special Issue Mechanisms and Interventions for Neurological and Psychological Disorders)

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23 pages, 2244 KiB

Open AccessReview

Alzheimer’s Disease: An Updated Overview of Its Genetics

by Jesús Andrade-Guerrero, Alberto Santiago-Balmaseda, Paola Jeronimo-Aguilar, Isaac Vargas-Rodríguez, Ana Ruth Cadena-Suárez, Carlos Sánchez-Garibay, Glustein Pozo-Molina, Claudia Fabiola Méndez-Catalá, Maria-del-Carmen Cardenas-Aguayo, Sofía Diaz-Cintra, Mar Pacheco-Herrero, José Luna-Muñoz and Luis O. Soto-Rojas

Int. J. Mol. Sci. 2023, 24(4), 3754; https://doi.org/10.3390/ijms24043754 - 13 Feb 2023

Cited by 48 | Viewed by 8715

Abstract

Alzheimer’s disease (AD) is the most common neurodegenerative disease in the world. It is classified as familial and sporadic. The dominant familial or autosomal presentation represents 1–5% of the total number of cases. It is categorized as early onset (EOAD; <65 years of age) and presents genetic mutations in presenilin 1 (PSEN1), presenilin 2 (PSEN2), or the Amyloid precursor protein (APP). Sporadic AD represents 95% of the cases and is categorized as late-onset (LOAD), occurring in patients older than 65 years of age. Several risk factors have been identified in sporadic AD; aging is the main one. Nonetheless, multiple genes have been associated with the different neuropathological events involved in LOAD, such as the pathological processing of Amyloid beta (Aβ) peptide and Tau protein, as well as synaptic and mitochondrial dysfunctions, neurovascular alterations, oxidative stress, and neuroinflammation, among others. Interestingly, using genome-wide association study (GWAS) technology, many polymorphisms associated with LOAD have been identified. This review aims to analyze the new genetic findings that are closely related to the pathophysiology of AD. Likewise, it analyzes the multiple mutations identified to date through GWAS that are associated with a high or low risk of developing this neurodegeneration. Understanding genetic variability will allow for the identification of early biomarkers and opportune therapeutic targets for AD. Full article

(This article belongs to the Special Issue Mechanisms and Interventions for Neurological and Psychological Disorders)

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46 pages, 6854 KiB

Open AccessReview

Experimental and Clinical Biomarkers for Progressive Evaluation of Neuropathology and Therapeutic Interventions for Acute and Chronic Neurological Disorders

by Doodipala Samba Reddy and Hasara Nethma Abeygunaratne

Int. J. Mol. Sci. 2022, 23(19), 11734; https://doi.org/10.3390/ijms231911734 - 03 Oct 2022

Cited by 14 | Viewed by 4369

Abstract

This article describes commonly used experimental and clinical biomarkers of neuronal injury and neurodegeneration for the evaluation of neuropathology and monitoring of therapeutic interventions. Biomarkers are vital for diagnostics of brain disease and therapeutic monitoring. A biomarker can be objectively measured and evaluated as a proxy indicator for the pathophysiological process or response to therapeutic interventions. There are complex hurdles in understanding the molecular pathophysiology of neurological disorders and the ability to diagnose them at initial stages. Novel biomarkers for neurological diseases may surpass these issues, especially for early identification of disease risk. Validated biomarkers can measure the severity and progression of both acute neuronal injury and chronic neurological diseases such as epilepsy, migraine, Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, traumatic brain injury, amyotrophic lateral sclerosis, multiple sclerosis, and other brain diseases. Biomarkers are deployed to study progression and response to treatment, including noninvasive imaging tools for both acute and chronic brain conditions. Neuronal biomarkers are classified into four core subtypes: blood-based, immunohistochemical-based, neuroimaging-based, and electrophysiological biomarkers. Neuronal conditions have progressive stages, such as acute injury, inflammation, neurodegeneration, and neurogenesis, which can serve as indices of pathological status. Biomarkers are critical for the targeted identification of specific molecules, cells, tissues, or proteins that dramatically alter throughout the progression of brain conditions. There has been tremendous progress with biomarkers in acute conditions and chronic diseases affecting the central nervous system. Full article

(This article belongs to the Special Issue Mechanisms and Interventions for Neurological and Psychological Disorders)

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18 pages, 371 KiB

Open AccessReview

The Role of Tryptophan Metabolites in Neuropsychiatric Disorders

by Majid Davidson, Niloufar Rashidi, Kulmira Nurgali and Vasso Apostolopoulos

Int. J. Mol. Sci. 2022, 23(17), 9968; https://doi.org/10.3390/ijms23179968 - 01 Sep 2022

Cited by 31 | Viewed by 5035

Abstract

In recent decades, neuropsychiatric disorders such as major depressive disorder, schizophrenia, bipolar, etc., have become a global health concern, causing various detrimental influences on patients. Tryptophan is an important amino acid that plays an indisputable role in several physiological processes, including neuronal function and immunity. Tryptophan’s metabolism process in the human body occurs using different pathways, including the kynurenine and serotonin pathways. Furthermore, other biologically active components, such as serotonin, melatonin, and niacin, are by-products of Tryptophan pathways. Current evidence suggests that a functional imbalance in the synthesis of Tryptophan metabolites causes the appearance of pathophysiologic mechanisms that leads to various neuropsychiatric diseases. This review summarizes the pharmacological influences of tryptophan and its metabolites on the development of neuropsychiatric disorders. In addition, tryptophan and its metabolites quantification following the neurotransmitters precursor are highlighted. Eventually, the efficiency of various biomarkers such as inflammatory, protein, electrophysiological, genetic, and proteomic biomarkers in the diagnosis/treatment of neuropsychiatric disorders was discussed to understand the biomarker application in the detection/treatment of various diseases. Full article

(This article belongs to the Special Issue Mechanisms and Interventions for Neurological and Psychological Disorders)

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