Neurodegeneration No More: Cutting-Edge Technologies and Therapies in the Evolution of Neurodegenerative Disease Management

A topical collection in Biomedicines (ISSN 2227-9059). This collection belongs to the section "Neurobiology and Clinical Neuroscience".

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Editors


E-Mail Website
Collection Editor
HUN-REN-SZTE Neuroscience Research Group, Hungarian Research Network, University of Szeged (HUN-REN-SZTE), Szeged, Hungary
Interests: neurohormones; neuropeptides; tryptophan; kynurenine; psychiatry; neurology; depression; anxiety; dementia; pain; Alzheimer’s disease; cognition; antidepressant; translational research
Special Issues, Collections and Topics in MDPI journals

E-Mail Website1 Website2
Collection Editor
1. Department of Psychology, University of Turin, Turin, Italy
2. Center for Studies and Research in Cognitive Neuroscience, Department of Psychology, University of Bologna, Bologna, Italy
Interests: NIBS techniques; TMS; skin conductance; heart rate variability; fear conditioning; fear learning; learning; neuropsychology; prefrontal cortex; amygdala; hippocampus; anxiety; depression; working memory; PTSD; skin conductance responses; psychophysiology; error-related negativity; EEG; tDCS; Alzheimer’s disease; PIT; stress-related disorders; Parkinson’s disease; resilience; memory; neurologic patients; cognitive decisions; fMRI; translational and molecular psychiatry
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Collection Editor
Department of Psychology, University of Turin, Turin, Italy
Interests: magnetic resonance imaging; human brain mapping; meta-research; connectomics; brain connectivity; computational neuroscience; Bayesian statistics; fMRI; meta-analysis; clinical trials; DTI; default mode network; Alzheimer’s disease; biological psychiatry; autism; cerebellum; translational neuroimaging

Topical Collection Information

Dear Colleagues,

Neurodegenerative diseases are a group of disorders that affect the structure and function of the central nervous system, leading to the progressive loss of cognitive, motor, and sensory abilities. They include Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, Huntington’s disease, and many others. Neurodegenerative diseases pose a major challenge for public health as they affect millions of people worldwide and have no cure. Moreover, they are associated with a high burden of disability, morbidity, mortality, and socioeconomic costs.

In recent years, significant advances have been made in the understanding of the pathophysiology, epidemiology, and genetics of neurodegenerative diseases, as well as in the development of novel diagnostic tools, therapeutic interventions, and rehabilitation strategies. Non-invasive brain stimulation (NIBS) techniques, such as transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (tDCS), have shown potential to improve both motor and nonmotor symptoms in patients with neurodegenerative diseases like Alzheimer’s and Parkinson’s. These techniques are of particular interest for the treatment of cognitive impairment in Alzheimer’s disease and axial disturbances in Parkinson’s disease, where conventional pharmacological therapies have shown limited effects. Recent evidence suggests that NIBS may have a neuroprotective effect, potentially slowing disease progression and modulating the aggregation state of pathological proteins. However, many gaps and challenges remain in the field, such as the identification of reliable biomarkers, the elucidation of the environmental and lifestyle factors that modulate disease risk and progression, the optimization of clinical trials and drug delivery systems, and improvements in the quality of life and care of patients and caregivers. Moreover, the potential of NIBS to influence disease progression over time remains poorly understood, along with ongoing investigations into the development of standardized stimulation protocols for the precise targeting of deep brain regions.

This Topical Collection aims to showcase the latest research and innovations in the field of neurodegenerative diseases, covering a wide range of topics, such as the following:

  • Risk factors, such as genetic and environmental, that influence the onset and course of neurodegenerative diseases;
  • Prodromal symptoms and early diagnosis, using advanced imaging techniques, biomarkers, and digital technologies;
  • Comorbidities, such as psychiatric, metabolic, and cardiovascular disorders, that affect or are affected by neurodegenerative diseases;
  • Novel therapeutic targets and treatments, such as gene therapy, stem cell therapy, immunotherapy, medicinal plants, phytocompounds, and neuroprotective agents;
  • Role of oxidative stress and inflammation as triggers of neurodegenerative conditions;
  • Quality-of-life-oriented rehabilitation, such as cognitive, physical, and psychosocial interventions that enhance the functioning and well-being of patients and caregivers;
  • Innovative translational research, such as bench-to-bed and bed-to-bench, and modeling, such as in vitro and in vivo;
  • Non-invasive brain stimulation (NIBS) as a therapeutic intervention that may offer neuroprotective effects and improve symptoms in neurodegenerative diseases.

We invite researchers and clinicians from various disciplines and backgrounds to submit their original articles and reviews to this Topical Collection contribute to the advancement of knowledge and practice in the field of neurodegenerative diseases. We hope that this Topical Collection will provide a comprehensive and up-to-date overview of the current state and future directions of the field and will stimulate further research and collaboration among the scientific community.

Dr. Masaru Tanaka
Dr. Simone Battaglia
Dr. Donato Liloia
Collection Editor

Manuscript Submission Information

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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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

  • Alzheimer’s disease
  • frontotemporal lobar degeneration
  • Parkinson’s disease
  • aging decline
  • mild cognitive impairment
  • multiple sclerosis
  • stroke
  • acquired brain damage
  • altered cognitive processes
  • brain functional impairment
  • neurocognitive disorders
  • cognitive, behavioral, and functional disorders
  • acquired trauma
  • brain plasticity and connectivity
  • non-invasive brain stimulation
  • diagnosis and treatment
  • functional evidence of altered cognition and connectivity
  • blood-based biomarkers
  • disease heterogeneity
  • prognosis
  • protein aggregation
  • inflammation
  • oxidative stress
  • medicinal plants
  • phytocompounds

Published Papers (4 papers)

2024

20 pages, 505 KiB  
Article
Mitochondrial Dysfunction in Sporadic Amyotrophic Lateral Sclerosis Patients: Insights from High-Resolution Respirometry
by Petra Parvanovova, Andrea Evinova, Milan Grofik, Petra Hnilicova, Zuzana Tatarkova and Monika Turcanova-Koprusakova
Biomedicines 2024, 12(6), 1294; https://doi.org/10.3390/biomedicines12061294 - 11 Jun 2024
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Abstract
Amyotrophic lateral sclerosis is a severe neurodegenerative disease whose exact cause is still unclear. Currently, research attention is turning to the mitochondrion as a critical organelle of energy metabolism. Current knowledge is sufficient to confirm the involvement of the mitochondria in the pathophysiology [...] Read more.
Amyotrophic lateral sclerosis is a severe neurodegenerative disease whose exact cause is still unclear. Currently, research attention is turning to the mitochondrion as a critical organelle of energy metabolism. Current knowledge is sufficient to confirm the involvement of the mitochondria in the pathophysiology of the disease, since the mitochondria are involved in many processes in the cell; however, the exact mechanism of involvement is still unclear. We used peripheral blood mononuclear cells isolated from whole fresh blood from patients with amyotrophic lateral sclerosis for measurement and matched an age- and sex-matched set of healthy subjects. The group of patients consisted of patients examined and diagnosed at the neurological clinic of the University Hospital Martin. The set of controls consisted of healthy individuals who were actively searched, and controls were selected on the basis of age and sex. The group consisted of 26 patients with sporadic forms of ALS (13 women, 13 men), diagnosed based on the definitive criteria of El Escorial. The average age of patients was 54 years, and the average age of healthy controls was 56 years. We used a high-resolution O2K respirometry method, Oxygraph-2k, to measure mitochondrial respiration. Basal respiration was lower in patients by 29.48%, pyruvate-stimulated respiration (respiratory chain complex I) was lower by 29.26%, and maximal respiratory capacity was lower by 28.15%. The decrease in succinate-stimulated respiration (respiratory chain complex II) was 26.91%. Our data confirm changes in mitochondrial respiration in ALS patients, manifested by the reduced function of complex I and complex II of the respiratory chain. These defects are severe enough to confirm this disease’s hypothesized mitochondrial damage. Therefore, research interest in the future should be directed towards a deeper understanding of the involvement of mitochondria and respiratory complexes in the pathophysiology of the disease. This understanding could develop new biomarkers in diagnostics and subsequent therapeutic interventions. Full article
14 pages, 883 KiB  
Article
Oxytocin and Vasopressin Gene Expression in the Brain as Potential Biomarkers for Cannabidiol Therapeutic Efficacy
by Christa M. Frodella, Stephen B. Pruett, Matthew K. Ross and Barbara L. F. Kaplan
Biomedicines 2024, 12(6), 1273; https://doi.org/10.3390/biomedicines12061273 - 7 Jun 2024
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Abstract
Over the last several years, there has been increased interest in cannabidiol (CBD) to treat various ailments such as pain, anxiety, insomnia, and inflammation. The potential for CBD as an anti-inflammatory therapy has come, in part, from its demonstrated ability to suppress neuroinflammation [...] Read more.
Over the last several years, there has been increased interest in cannabidiol (CBD) to treat various ailments such as pain, anxiety, insomnia, and inflammation. The potential for CBD as an anti-inflammatory therapy has come, in part, from its demonstrated ability to suppress neuroinflammation in autoimmune diseases, such as the mouse model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE). The increased use of CBD strongly suggests that more research is necessary to elucidate its safety and efficacy and determine the mechanisms by which it acts. Thus, we conducted two separate studies. In the first, RNA sequencing (RNA-Seq) analysis of brains of female mice undergoing EAE in the presence and absence of CBD was conducted to identify potential genes that mediated its neuroprotective effects when efficacious. In the second, we assessed some of the same genes in male and female mice treated with CBD in the absence of an immune stimulus. Together, these data showed that CBD modestly increased oxytocin (Oxt) and arginine vasopressin (vasopressin, Avp) gene expression in the brains of mice, regardless of whether there was active inflammation. Overall, these data suggest that Oxt and Avp might act as biomarkers for CBD exposure. Full article
12 pages, 3617 KiB  
Article
Mild Disease Course of Experimental Autoimmune Encephalomyelitis without Pertussis Toxin: Brain Transcriptome Analysis Reveals Similar Signaling to Active Lesions in Multiple Sclerosis
by Christa M. Frodella, Stephen B. Pruett and Barbara L. F. Kaplan
Biomedicines 2024, 12(6), 1215; https://doi.org/10.3390/biomedicines12061215 - 30 May 2024
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Abstract
Experimental autoimmune encephalomyelitis (EAE) is a powerful model to study multiple sclerosis (MS). One of the approaches for EAE is to actively immunize with myelin-derived peptides with immune adjuvants. One of the commonly used immune adjuvants is pertussis toxin (PTx), without which EAE [...] Read more.
Experimental autoimmune encephalomyelitis (EAE) is a powerful model to study multiple sclerosis (MS). One of the approaches for EAE is to actively immunize with myelin-derived peptides with immune adjuvants. One of the commonly used immune adjuvants is pertussis toxin (PTx), without which EAE disease is mild with relatively longer onset. However, pertussis toxin can also inhibit G protein-coupled receptor (GPCR) signaling so it can confound investigations into the role of GPCRs in EAE or therapies designed to target GPCRs. Since EAE via active immunization without PTx results in a relatively mild disease state, we wanted to confirm that appropriate signaling molecules for the disease were being induced in one target tissue (i.e., brain). RNA-Seq analysis of whole brain tissue demonstrated that the MS signaling pathway was strongly activated in symptomatic mice. In addition, there was activation of Th1 (IFN signaling), Th2 (IL-4 signaling), and Th17 (IL-17 signaling). In comparing canonical pathways from our mouse mild EAE brains with a human MS atlas, EAE shared the most pathways with active and inactive lesions. An advantage of this approach is that disease induction is slower to develop and results in modest clinical signs, which likely more closely mimic human disease onset. Full article
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17 pages, 3161 KiB  
Article
Comparison of Protective Effects of Antidepressants Mediated by Serotonin Receptor in Aβ-Oligomer-Induced Neurotoxicity
by Ken Yamamoto, Mayumi Tsuji, Tatsunori Oguchi, Yutaro Momma, Hideaki Ohashi, Naohito Ito, Tetsuhito Nohara, Tatsuya Nakanishi, Atsushi Ishida, Masahiro Hosonuma, Toru Nishikawa, Hidetomo Murakami and Yuji Kiuchi
Biomedicines 2024, 12(6), 1158; https://doi.org/10.3390/biomedicines12061158 - 23 May 2024
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Abstract
Amyloid β-peptide (Aβ) synthesis and deposition are the primary factors underlying the pathophysiology of Alzheimer’s disease (AD). Aβ oligomer (Aβo) exerts its neurotoxic effects by inducing oxidative stress and lesions by adhering to cellular membranes. Though several antidepressants have been investigated as neuroprotective [...] Read more.
Amyloid β-peptide (Aβ) synthesis and deposition are the primary factors underlying the pathophysiology of Alzheimer’s disease (AD). Aβ oligomer (Aβo) exerts its neurotoxic effects by inducing oxidative stress and lesions by adhering to cellular membranes. Though several antidepressants have been investigated as neuroprotective agents in AD, a detailed comparison of their neuroprotection against Aβo-induced neurotoxicity is lacking. Here, we aimed to elucidate the neuroprotective effects of clinically prescribed selective serotonin reuptake inhibitors, serotonin–norepinephrine reuptake inhibitors, and noradrenergic and specific serotonergic antidepressants at the cellular level and establish the underlying mechanisms for their potential clinical applications. Therefore, we compared the neuroprotective effects of three antidepressants, fluoxetine (Flx), duloxetine (Dlx), and mirtazapine (Mir), by their ability to prevent oxidative stress-induced cell damage, using SH-SY5Y cells, by evaluating cell viability, generation of reactive oxygen species (ROS) and mitochondrial ROS, and peroxidation of cell membrane phospholipids. These antidepressants exhibited potent antioxidant activity (Dlx > Mir > Flx) and improved cell viability. Furthermore, pretreatment with a 5-hydroxytryptamine 1A (5-HT1A) antagonist suppressed their effects, suggesting that the 5-HT1A receptor is involved in the antioxidant mechanism of the antidepressants’ neuroprotection. These findings suggest the beneficial effects of antidepressant treatment in AD through the prevention of Aβ-induced oxidative stress. Full article
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