Emerging Translational Research in Neurological and Psychiatric Diseases: From In Vitro to In Vivo Models, from Animals to Humans, from Qualitative to Quantitative Methods, 3rd Edition

Topic Information

Dear Colleagues,

Translational research is a crucial and complex field in laboratory sciences that focuses on understanding the underlying mechanisms, searching for biomarkers, and developing therapeutics for neurological and psychiatric disorders. It involves integrating knowledge from basic neuroscience with the development of diagnostic and therapeutic tools that can be applied in clinical practice. The following are some key points on translational research in neurologic and psychiatric diseases:

1. Understanding Pathomechanisms: Translational research aims to uncover the underlying pathomechanisms of neurological and psychiatric disorders. This involves studying the molecular factors and neural computations that contribute to brain impairments and mental disorders.
2. Biomarker Discovery: Translational research also focuses on searching for new biomarkers that can aid in the diagnosis, prognosis, and monitoring of these diseases. Biomarkers, such as microRNAs, can provide valuable information about disease progression and treatment response.
3. Therapeutic Development: Another important aspect of translational research is the development of novel therapeutics for neurological and psychiatric disorders or the repurposing of drugs. This involves identifying potential targets and testing new treatment approaches in preclinical and clinical settings.
4. Disease Models: In vivo and in vitro disease models play a significant role in translational research. These models help researchers understand the complex polygenic, multifactorial, and heterogeneous disease mechanisms associated with neurological and psychiatric disorders.
5. Sex/Gender and Ageing: Emerging research in translational neuroscience has highlighted the intriguing interaction of sex/gender and aging with the pathogenesis of neuropsychiatric diseases. Understanding these factors can lead to more personalized and effective treatments.
6. Disease Range: Translational research encompasses a wide range of diseases, including Alzheimer's disease, Parkinson's disease, multiple sclerosis, Huntington's disease, amyotrophic lateral sclerosis, stroke sequelae, HIV infection, and various psychiatric disorders.

The Special Issue mentioned in the invitation focuses on the latest developments in translational research in neurologic and psychiatric diseases. It aims to highlight the progress made in understanding these diseases and developing new approaches for diagnosis, treatment, and personalized medicine. Translational research plays a crucial role in bridging the gap between basic scientific knowledge and clinical practice, with the ultimate goal of improving the lives of individuals affected by neurological and psychiatric disorders. This Special Issue aims to shed light on the latest research pertaining to the comorbidity of depression, anxiety, dementia, and chronic pain in various diseases.

We cordially invite authors to contribute original research articles focusing on, but not limited to, the following:

• Etiology, pathogenesis, and progression mechanisms;
• Early diagnosis including biomarkers, bio-imaging, biosensors, neuroimaging;
• Methodology;
• Biomaterial biomedical research;
• Prophylactic, disease-modifying, and therapeutic strategies; novel targets;
• Novel drug discovery and development, naturally driven biomedicines, natural bioactive molecules, and vaccines;
• Antidepressants, anti-anxiolytics, cognitive enhancers, analgesics;
• Novel targets in various therapeutic areas: cardiovascular, vascular, hematology, oncology, neurology, orthopedics, dermatology, ophthalmology, and other peripheral systems;
• The repurposing of drugs;
• Biopharmaceutical biomedicine, biologics, biosimilars, nanobiotechnology, nanosimilars, and nanobiosimilars;
• Nanoscaffold implants (synthetic vascular graft), and biosensors;
• Bioimaging, gene therapy, vaccine, cell therapy, and tissue engineering;
• Predictors of clinical treatment responses;
• Preclinical in vitro models, and animal models;
• Bench-to-bedside translation research;
• Bedside-to-bench translational research.
• Computational neuroscience, and computational psychiatry.

Review articles including expert opinions, systematic analysis, metanalysis, and other statistical and analytical methods are also welcome.

Dr. Masaru Tanaka
Dr. Lydia Giménez-Llort
Dr. Simone Battaglia
Topic Editors

Keywords

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Biomedicines biomedicines	3.9	5.2	2013	15.3 Days	CHF 2600	Submit
Biomolecules biomolecules	4.8	9.4	2011	16.3 Days	CHF 2700	Submit
Brain Sciences brainsci	2.7	4.8	2011	12.9 Days	CHF 2200	Submit
Cells cells	5.1	9.9	2012	17.5 Days	CHF 2700	Submit
International Journal of Molecular Sciences ijms	4.9	8.1	2000	18.1 Days	CHF 2900	Submit

MDPI Topics is cooperating with Preprints.org and has built a direct connection between MDPI journals and Preprints.org. Authors are encouraged to enjoy the benefits by posting a preprint at Preprints.org prior to publication:

1. Immediately share your ideas ahead of publication and establish your research priority;
2. Protect your idea from being stolen with this time-stamped preprint article;
3. Enhance the exposure and impact of your research;
4. Receive feedback from your peers in advance;
5. Have it indexed in Web of Science (Preprint Citation Index), Google Scholar, Crossref, SHARE, PrePubMed, Scilit and Europe PMC.

Related Topic

Published Papers (7 papers)

Order results

Content type Publication Date

Result details

Normal Extended Compact

Journals

All Biomedicines Biomolecules Brain Sciences Cells IJMS

Show export options expand_more Show export options expand_less

Select all

Export citation of selected articles as:

Plain Text BibTeX BibTeX (without abstracts) Endnote Endnote (without abstracts) Tab-delimited RIS

Error

Oops... you haven't selected anything for export.

Ok

clear

attachment

Supplementary material:
Supplementary File 1 (ZIP, 850 KiB)

20 pages, 5586 KiB  

Open AccessArticle

Impact of Serotonin Transporter Absence on Brain Insulin Receptor Expression, Plasma Metabolome Changes, and ADHD-like Behavior in Mice fed a Western Diet

by Daniel C. Anthony, Fay Probert, Anna Gorlova, Jenna Hebert, Daniel Radford-Smith, Zlata Nefedova, Aleksei Umriukhin, Andrey Nedorubov, Raymond Cespuglio, Boris Shulgin, Aleksey Lyundup, Klaus Peter Lesch and Tatyana Strekalova

Biomolecules 2024, 14(8), 884; https://doi.org/10.3390/biom14080884 - 23 Jul 2024

Viewed by 525

Abstract

The impaired function of the serotonin transporter (SERT) in humans has been linked to a higher risk of obesity and type 2 diabetes, especially as people age. Consuming a “Western diet” (WD), which is high in saturated fats, cholesterol, and sugars, can induce [...] Read more.

The impaired function of the serotonin transporter (SERT) in humans has been linked to a higher risk of obesity and type 2 diabetes, especially as people age. Consuming a “Western diet” (WD), which is high in saturated fats, cholesterol, and sugars, can induce metabolic syndrome. Previous research indicated that mice carrying a targeted inactivation of the Sert gene (knockout, KO) and fed a WD display significant metabolic disturbances and behaviors reminiscent of ADHD. These abnormalities might be mediated via a dysfunction in insulin receptor (IR) signaling, which is also associated with adult ADHD. However, the impact of Sert deficiency on IR signaling and systemic metabolic changes has not been thoroughly explored. In this study, we conducted a detailed analysis of locomotor behavior in wild-type (WT) and KO mice fed a WD or control diet. We investigated changes in the blood metabolome and examined, via PCR, the expression of insulin receptor A and B isoforms and key regulators of their function in the brain. Twelve-month-old KO mice and their WT littermates were fed a WD for three weeks. Nuclear magnetic resonance spectroscopy analysis of plasma samples showed that KO mice on a WD had higher levels of lipids and lipoproteins and lower levels of glucose, lactate, alanine, valine, and isoleucine compared to other groups. SERT-KO mice on the control diet exhibited increased brain levels of both IR A and B isoforms, accompanied by a modest increase in the negative regulator ENPP. The KO mice also displayed anxiety-like behavior and reduced exploratory activity in an open field test. However, when the KO animals were fed a WD, the aberrant expression levels of IR isoforms in the KO mice and locomotor behavior were ameliorated indicating a complex interaction between genetic and dietary factors that might contribute to ADHD-like symptoms. Overall, our findings suggest that the lack of Sert leads to a unique metabolic phenotype in aged mice, characterized by dysregulated IR-related pathways. These changes are exacerbated by WD in the blood metabolome and are associated with behavioral abnormalities. Full article

(This article belongs to the Topic Emerging Translational Research in Neurological and Psychiatric Diseases: From In Vitro to In Vivo Models, from Animals to Humans, from Qualitative to Quantitative Methods, 3rd Edition)

►▼ Show Figures

Figure 1

21 pages, 360 KiB  

Open AccessReview

Psychiatric Disease as a Potential Risk Factor for Dementia: A Narrative Review

by Dawson W. Hedges, Morgan Chase, Thomas J. Farrer and Shawn D. Gale

Brain Sci. 2024, 14(7), 722; https://doi.org/10.3390/brainsci14070722 - 18 Jul 2024

Viewed by 638

Abstract

Neurodegenerative disease is a major global health problem with 150 million people predicted to have dementia by 2050. Genetic factors, environmental factors, demographics, and some diseases have been associated with dementia. In addition to associations between diseases such as hypertension and cerebrovascular disease [...] Read more.

Neurodegenerative disease is a major global health problem with 150 million people predicted to have dementia by 2050. Genetic factors, environmental factors, demographics, and some diseases have been associated with dementia. In addition to associations between diseases such as hypertension and cerebrovascular disease and dementia, emerging findings associate some psychiatric disorders with incident dementia. Because of the high and increasing global prevalence of dementia and the high worldwide prevalence of psychiatric disorders, the primary objective of this narrative review was to evaluate published findings that evaluate the association between bipolar disorder, depression, anxiety, post-traumatic stress disorder, obsessive–compulsive disorder, attention-deficit/hyperactivity disorder, autism spectrum disorder, schizophrenia and other psychosis syndromes, and personality disorders and personality traits and incident dementia. Here, we highlight findings indicating possible associations between these psychiatric disorders and subsequent dementia and suggest that some psychiatric disorders may be risk factors for incident dementia. Further research, including more large longitudinal studies and additional meta-analyses, however, is needed to better characterize the associations between psychiatric disorders and incident dementia, to identify possible mechanisms for these putative associations, and to identify risk factors within psychiatric disorders that predispose some people with a psychiatric disorder but not others to subsequent dementia. Additional important questions concern how the treatment of psychiatric disorders might affect the risk of incident dementia. Full article

(This article belongs to the Topic Emerging Translational Research in Neurological and Psychiatric Diseases: From In Vitro to In Vivo Models, from Animals to Humans, from Qualitative to Quantitative Methods, 3rd Edition)

20 pages, 5054 KiB  

Open AccessArticle

Brain–Bone Crosstalk in a Murine Polytrauma Model Promotes Bone Remodeling but Impairs Neuromotor Recovery and Anxiety-Related Behavior

by Katharina Ritter, Markus Baalmann, Christopher Dolderer, Ulrike Ritz and Michael K. E. Schäfer

Biomedicines 2024, 12(7), 1399; https://doi.org/10.3390/biomedicines12071399 - 24 Jun 2024

Viewed by 626

Abstract

Traumatic brain injury (TBI) and long bone fractures are a common injury pattern in polytrauma patients and modulate each other’s healing process. As only a limited number of studies have investigated both traumatic sites, we tested the hypothesis that brain–bone polytrauma mutually impacts [...] Read more.

Traumatic brain injury (TBI) and long bone fractures are a common injury pattern in polytrauma patients and modulate each other’s healing process. As only a limited number of studies have investigated both traumatic sites, we tested the hypothesis that brain–bone polytrauma mutually impacts neuro- and osteopathological outcomes. Adult female C57BL/6N mice were subjected to controlled cortical impact (CCI), and/or osteosynthetic stabilized femoral fracture (FF), or sham surgery. Neuromotor and behavioral impairments were assessed by neurological severity score, open field test, rotarod test, and elevated plus maze test. Brain and bone tissues were processed 42 days after trauma. CCI+FF polytrauma mice had increased bone formation as compared to FF mice and increased mRNA expression of bone sialoprotein (BSP). Bone fractures did not aggravate neuropathology or neuroinflammation assessed by cerebral lesion size, hippocampal integrity, astrocyte and microglia activation, and gene expression. Behavioral assessments demonstrated an overall impaired recovery of neuromotor function and persistent abnormalities in anxiety-related behavior in polytrauma mice. This study shows enhanced bone healing, impaired neuromotor recovery and anxiety-like behavior in a brain–bone polytrauma model. However, bone fractures did not aggravate TBI-evoked neuropathology, suggesting the existence of outcome-relevant mechanisms independent of the extent of brain structural damage and neuroinflammation. Full article

(This article belongs to the Topic Emerging Translational Research in Neurological and Psychiatric Diseases: From In Vitro to In Vivo Models, from Animals to Humans, from Qualitative to Quantitative Methods, 3rd Edition)

►▼ Show Figures

Graphical abstract

attachment

Supplementary material:
Supplementary File 1 (ZIP, 137 KiB)

20 pages, 3121 KiB  

Open AccessArticle

No Evidence of Sensory Neuropathy in a Traditional Mouse Model of Idiopathic Parkinson’s Disease

by Mahvish Faisal, Anna Rusetskaya, Liis Väli, Pille Taba, Ave Minajeva and Miriam A. Hickey

Cells 2024, 13(10), 799; https://doi.org/10.3390/cells13100799 - 8 May 2024

Viewed by 807

Abstract

Parkinson’s disease (PD) is the second-most common neurodegenerative disorder worldwide and is diagnosed based on motor impairments. Non-motor symptoms are also well-recognised in this disorder, and peripheral neuropathy is a frequent but poorly appreciated non-motor sign. Studying how central and peripheral sensory systems [...] Read more.

Parkinson’s disease (PD) is the second-most common neurodegenerative disorder worldwide and is diagnosed based on motor impairments. Non-motor symptoms are also well-recognised in this disorder, and peripheral neuropathy is a frequent but poorly appreciated non-motor sign. Studying how central and peripheral sensory systems are affected can contribute to the development of targeted therapies and deepen our understanding of the pathophysiology of PD. Although the cause of sporadic PD is unknown, chronic exposure to the pesticide rotenone in humans increases the risk of developing the disease. Here, we aimed to investigate whether peripheral neuropathy is present in a traditional model of PD. Mice receiving intrastriatal rotenone showed greatly reduced dopamine terminals in the striatum and a reduction in tyrosine hydroxylase-positive neurons in the Substantia nigra pars compacta and developed progressive motor impairments in hindlimb stepping and rotarod but no change in spontaneous activity. Interestingly, repeated testing using gold-standard protocols showed no change in gut motility, a well-known non-motor symptom of PD. Importantly, we did not observe any change in heat, cold, or touch sensitivity, again based upon repeated testing with well-validated protocols that were statistically well powered. Therefore, this traditional model fails to replicate PD, and our data again reiterate the importance of the periphery to the disorder. Full article

(This article belongs to the Topic Emerging Translational Research in Neurological and Psychiatric Diseases: From In Vitro to In Vivo Models, from Animals to Humans, from Qualitative to Quantitative Methods, 3rd Edition)

►▼ Show Figures

Figure 1

24 pages, 872 KiB  

Open AccessReview

Revolutionizing Ischemic Stroke Diagnosis and Treatment: The Promising Role of Neurovascular Unit-Derived Extracellular Vesicles

by Xiangyu Gao, Dan Liu, Kangyi Yue, Zhuoyuan Zhang, Xiaofan Jiang and Peng Luo

Biomolecules 2024, 14(3), 378; https://doi.org/10.3390/biom14030378 - 20 Mar 2024

Viewed by 2006

Abstract

Ischemic stroke is a fatal and disabling disease worldwide and imposes a significant burden on society. At present, biological markers that can be conveniently measured in body fluids are lacking for the diagnosis of ischemic stroke, and there are no effective treatment methods [...] Read more.

Ischemic stroke is a fatal and disabling disease worldwide and imposes a significant burden on society. At present, biological markers that can be conveniently measured in body fluids are lacking for the diagnosis of ischemic stroke, and there are no effective treatment methods to improve neurological function after ischemic stroke. Therefore, new ways of diagnosing and treating ischemic stroke are urgently needed. The neurovascular unit, composed of neurons, astrocytes, microglia, and other components, plays a crucial role in the onset and progression of ischemic stroke. Extracellular vesicles are nanoscale lipid bilayer vesicles secreted by various cells. The key role of extracellular vesicles, which can be released by cells in the neurovascular unit and serve as significant facilitators of cellular communication, in ischemic stroke has been extensively documented in recent literature. Here, we highlight the role of neurovascular unit-derived extracellular vesicles in the diagnosis and treatment of ischemic stroke, the current status of extracellular vesicle engineering for ischemic stroke treatment, and the problems encountered in the clinical translation of extracellular vesicle therapies. Extracellular vesicles derived from the neurovascular unit could provide an important contribution to diagnostic and therapeutic tools in the future, and more studies in this area should be carried out. Full article

(This article belongs to the Topic Emerging Translational Research in Neurological and Psychiatric Diseases: From In Vitro to In Vivo Models, from Animals to Humans, from Qualitative to Quantitative Methods, 3rd Edition)

►▼ Show Figures

Graphical abstract

attachment

Supplementary material:
Supplementary File 1 (ZIP, 244 KiB)

26 pages, 8503 KiB  

Open AccessArticle

The Impact of C-3 Side Chain Modifications on Kynurenic Acid: A Behavioral Analysis of Its Analogs in the Motor Domain

by Diána Martos, Bálint Lőrinczi, István Szatmári, László Vécsei and Masaru Tanaka

Int. J. Mol. Sci. 2024, 25(6), 3394; https://doi.org/10.3390/ijms25063394 - 16 Mar 2024

Cited by 5 | Viewed by 3493

Abstract

The central nervous system (CNS) is the final frontier in drug delivery because of the blood–brain barrier (BBB), which poses significant barriers to the access of most drugs to their targets. Kynurenic acid (KYNA), a tryptophan (Trp) metabolite, plays an important role in [...] Read more.

The central nervous system (CNS) is the final frontier in drug delivery because of the blood–brain barrier (BBB), which poses significant barriers to the access of most drugs to their targets. Kynurenic acid (KYNA), a tryptophan (Trp) metabolite, plays an important role in behavioral functions, and abnormal KYNA levels have been observed in neuropsychiatric conditions. The current challenge lies in delivering KYNA to the CNS owing to its polar side chain. Recently, C-3 side chain-modified KYNA analogs have been shown to cross the BBB; however, it is unclear whether they retain the biological functions of the parent molecule. This study examined the impact of KYNA analogs, specifically, SZR-72, SZR-104, and the newly developed SZRG-21, on behavior. The analogs were administered intracerebroventricularly (i.c.v.), and their effects on the motor domain were compared with those of KYNA. Specifically, open-field (OF) and rotarod (RR) tests were employed to assess motor activity and skills. SZR-104 increased horizontal exploratory activity in the OF test at a dose of 0.04 μmol/4 μL, while SZR-72 decreased vertical activity at doses of 0.04 and 0.1 μmol/4 μL. In the RR test, however, neither KYNA nor its analogs showed any significant differences in motor skills at either dose. Side chain modification affects affective motor performance and exploratory behavior, as the results show for the first time. In this study, we showed that KYNA analogs alter emotional components such as motor-associated curiosity and emotions. Consequently, drug design necessitates the development of precise strategies to traverse the BBB while paying close attention to modifications in their effects on behavior. Full article

(This article belongs to the Topic Emerging Translational Research in Neurological and Psychiatric Diseases: From In Vitro to In Vivo Models, from Animals to Humans, from Qualitative to Quantitative Methods, 3rd Edition)

►▼ Show Figures

Graphical abstract

26 pages, 1141 KiB  

Open AccessReview

Targeting Human Glucocorticoid Receptors in Fear Learning: A Multiscale Integrated Approach to Study Functional Connectivity

by Simone Battaglia, Chiara Di Fazio, Matteo Mazzà, Marco Tamietto and Alessio Avenanti

Int. J. Mol. Sci. 2024, 25(2), 864; https://doi.org/10.3390/ijms25020864 - 10 Jan 2024

Cited by 19 | Viewed by 2582

Abstract

Fear extinction is a phenomenon that involves a gradual reduction in conditioned fear responses through repeated exposure to fear-inducing cues. Functional brain connectivity assessments, such as functional magnetic resonance imaging (fMRI), provide valuable insights into how brain regions communicate during these processes. Stress, [...] Read more.

Fear extinction is a phenomenon that involves a gradual reduction in conditioned fear responses through repeated exposure to fear-inducing cues. Functional brain connectivity assessments, such as functional magnetic resonance imaging (fMRI), provide valuable insights into how brain regions communicate during these processes. Stress, a ubiquitous aspect of life, influences fear learning and extinction by changing the activity of the amygdala, prefrontal cortex, and hippocampus, leading to enhanced fear responses and/or impaired extinction. Glucocorticoid receptors (GRs) are key to the stress response and show a dual function in fear regulation: while they enhance the consolidation of fear memories, they also facilitate extinction. Accordingly, GR dysregulation is associated with anxiety and mood disorders. Recent advancements in cognitive neuroscience underscore the need for a comprehensive understanding that integrates perspectives from the molecular, cellular, and systems levels. In particular, neuropharmacology provides valuable insights into neurotransmitter and receptor systems, aiding the investigation of mechanisms underlying fear regulation and potential therapeutic targets. A notable player in this context is cortisol, a key stress hormone, which significantly influences both fear memory reconsolidation and extinction processes. Gaining a thorough understanding of these intricate interactions has implications in terms of addressing psychiatric disorders related to stress. This review sheds light on the complex interactions between cognitive processes, emotions, and their neural bases. In this endeavor, our aim is to reshape the comprehension of fear, stress, and their implications for emotional well-being, ultimately aiding in the development of therapeutic interventions. Full article

(This article belongs to the Topic Emerging Translational Research in Neurological and Psychiatric Diseases: From In Vitro to In Vivo Models, from Animals to Humans, from Qualitative to Quantitative Methods, 3rd Edition)

►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less

Select all

Export citation of selected articles as:

Plain Text BibTeX BibTeX (without abstracts) Endnote Endnote (without abstracts) Tab-delimited RIS

 

Error

Oops... you haven't selected anything for export.

Ok

clear

Displaying articles 1-7