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Brain Sciences
Special Issues
Brain Evolution, Development, and Diseases
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Brain Evolution, Development, and Diseases

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Molecular and Cellular Neuroscience".

Deadline for manuscript submissions: closed (15 July 2021) | Viewed by 20936

Special Issue Editor

Dr. Umberto di Porzio

E-Mail Website1 Website2
Guest Editor
Institute of Genetics and Biophysics "Adriano Buzzati Traverso", CNR, 80131 Naples, Italy
Interests: brain development; transcriptional regulation of neurogenesis; midbrain dopaminergic neurons; Parkinson’s disease; regenerative medicine in animal models; neural stem cells; cell reprogramming; miRNA; music in emotion and learning; human brain evolution
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

The characteristics observed in the adult brain reflect specific models of human brain development, which depend heavily on the environment, as well as genetic information. The development of the central nervous system requires the generation of a wide range of specialized neuronal and non-neuronal cells, in appropriate numbers, positions, and timing. Furthermore, precise connections between neurons and efficient communication between neuronal and non-neuronal groups must be established for the brain to exercise its functions. However, the human brain largely matures after birth, which gives rise to a prolonged period in which synaptic connections are established in the infant, who grows in a stimulating and enriched environment. This is possible because the expression of the genes involved in different functions is asynchronous, thus, laying the foundations of the great plasticity of the human brain and its ability to potentially promote rapid modification of neuronal connectivity in response to new needs. However, genes that are involved in the development of the human brain and make it different from the brains of great apes may also be genes that can increase the risk of diseases, as diseases of aging. The latter appear after reproduction and are thus ignored by the pressure of natural selection.

We need to acquire new scientific evidence to study the possible disease mechanisms and identify new effective therapeutic strategies for the treatment of neurodegenerative and of a multitude of neurodevelopmental disorders.

This Special Issue will bring together the most recent studies aimed at unraveling the molecular and cellular mechanisms that regulate CNS development, maintenance of specific neuronal functions, and that illustrate the state of the art in new approaches for understanding human brain illnesses, linked to the discovery of genes implicated in the human brain evolution. We aim to link evolutionary selection, genetic variation to the development, and the functioning of neural circuits and diseases.

We welcome original research, reviews, and short reports, as well as technical reports on novel or improved experimental approaches or imaging tools aimed at identifying the cohort and the network of genes, involved in various aspects of CNS development under normal and pathological conditions, and how the latter can be modeled using animal or in vitro systems. Contributions that aim at elucidating determinants of selective neuronal vulnerability in some diseases, such as Parkinson’s Disease, Huntington, ALS, etc. with particular emphasis on the molecular and cellular alterations and their pathogenesis, are also welcome.

Dr. Umberto di Porzio
Guest Editor

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. Brain Sciences 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 2200 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

  • neurogenesis
  • synaptogenesis
  • neuronal connectivity
  • plasticity
  • enhancer
  • stem cell
  • organoids
  • brain genomics
  • music
  • culture
  • neurodegeneration
  • neurodevelopmental diseases

Published Papers (7 papers)

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Research

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15 pages, 5056 KiB  
Article
Influence of Topiramate on the Synaptic Endings of the Temporal Lobe Neocortex in an Experimental Model of Hyperthermia-Induced Seizures: An Ultrastructural Study
by Piotr Sobaniec, Joanna Maria Lotowska, Maria Elzbieta Sobaniec-Lotowska and Milena Zochowska-Sobaniec
Brain Sci. 2021, 11(11), 1433; https://0-doi-org.brum.beds.ac.uk/10.3390/brainsci11111433 - 28 Oct 2021
Cited by 2 | Viewed by 1637
Abstract
The objective of this pioneering study was to assess potentially neuroprotective properties of topiramate (TPM), a broad spectrum and newer-generation antiepileptic used against damage to synaptic endings of the temporal lobe neocortex in experimental hyperthermia-induced seizures (HS). TPM (80 mg/kg b.m.) was administered [...] Read more.
The objective of this pioneering study was to assess potentially neuroprotective properties of topiramate (TPM), a broad spectrum and newer-generation antiepileptic used against damage to synaptic endings of the temporal lobe neocortex in experimental hyperthermia-induced seizures (HS). TPM (80 mg/kg b.m.) was administered in young male Wistar rats with an intragastric tube before and immediately after HS. Specimens (1 mm3) collected from the neocortex, fixed via transcardial perfusion with paraformaldehyde and glutaraldehyde solution, were routinely processed for transmission-electron microscopic study, i.e., for descriptive and morphometric analysis. The ultrastructure of neocortical neuropil components affected by hyperthermic stress showed distinct swelling of pre and post-synaptic axodendritic and axospinal endings, including total disintegration. Mitochondria were markedly damaged in synaptic structures. Axoplasm of presynaptic boutons contained a decreased number of synaptic vesicles. Synaptic junctions showed active zone-shortening. Preventive administration of TPM before HS induction demonstrated neuroprotective effects against synaptic damage in approximately 1/4 of these structures. Interestingly, beneficial effects on synapsis morphology were more common in perivascular zones close to well-preserved capillaries. They were demonstrated by smaller swelling of both presynaptic and postsynaptic parts, well-preserved mitochondria, an increased number and regular distribution of synaptic vesicles within axoplasm, and a significantly increased synaptic active zones. However, topiramate used directly after HS was ineffective in the prevention of hyperthermia-evoked synaptic injury. Our findings support the hypothesis that topiramate applied before HS can protect some neocortical synapses via the vascular factor by enhancing blood–brain barrier components and improving the blood supply of gray matter in the temporal lobe, which may be significant in febrile seizure-prevention in children. Full article
(This article belongs to the Special Issue Brain Evolution, Development, and Diseases)
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13 pages, 2274 KiB  
Article
Oxidative Stress and Neurodevelopmental Outcomes in Rat Offspring with Intrauterine Growth Restriction Induced by Reduced Uterine Perfusion
by Marcelo E. Rains, Colin B. Muncie, Yi Pang, Lir-Wan Fan, Lu-Tai Tien and Norma B. Ojeda
Brain Sci. 2021, 11(1), 78; https://0-doi-org.brum.beds.ac.uk/10.3390/brainsci11010078 - 08 Jan 2021
Cited by 11 | Viewed by 2040
Abstract
Intrauterine growth restriction (IUGR) is a major cause of morbidity and mortality and is worldwide associated with delayed neurodevelopment. The exact mechanism involved in delayed neurodevelopment associated with IUGR is still unclear. Reduced uterine perfusion (RUP) is among the main causes of placental [...] Read more.
Intrauterine growth restriction (IUGR) is a major cause of morbidity and mortality and is worldwide associated with delayed neurodevelopment. The exact mechanism involved in delayed neurodevelopment associated with IUGR is still unclear. Reduced uterine perfusion (RUP) is among the main causes of placental insufficiency leading to IUGR, which is associated with increases in oxidative stress. This study investigated whether oxidative stress is associated with delayed neurodevelopment in IUGR rat pups. Pregnant rats were exposed to RUP surgery on gestational day 14 to generate IUGR rat offspring. We evaluated offspring’s morphometric at birth, and neurodevelopment on postnatal day 21 (PD21) as well as markers of oxidative stress in plasma and brain. Offspring from dams exposed to RUP showed significant (p < 0.05) lower birth weight compared to controls, indicating IUGR. Motor and cognitive deficits, and levels of oxidative stress markers, were significantly (p < 0.05) elevated in IUGR offspring compared to controls. IUGR offspring showed significant (p < 0.05) negative correlations between brain lipid peroxidation and neurocognitive tests (open field and novel object recognition) in comparison with controls. Our findings suggest that neurodevelopmental delay observed in IUGR rat offspring is associated with increased levels of oxidative stress markers. Full article
(This article belongs to the Special Issue Brain Evolution, Development, and Diseases)
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Review

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22 pages, 2080 KiB  
Review
Coenzyme a Biochemistry: From Neurodevelopment to Neurodegeneration
by Luca Mignani, Barbara Gnutti, Daniela Zizioli and Dario Finazzi
Brain Sci. 2021, 11(8), 1031; https://0-doi-org.brum.beds.ac.uk/10.3390/brainsci11081031 - 02 Aug 2021
Cited by 14 | Viewed by 4120
Abstract
Coenzyme A (CoA) is an essential cofactor in all living organisms. It is involved in a large number of biochemical processes functioning either as an activator of molecules with carbonyl groups or as a carrier of acyl moieties. Together with its thioester derivatives, [...] Read more.
Coenzyme A (CoA) is an essential cofactor in all living organisms. It is involved in a large number of biochemical processes functioning either as an activator of molecules with carbonyl groups or as a carrier of acyl moieties. Together with its thioester derivatives, it plays a central role in cell metabolism, post-translational modification, and gene expression. Furthermore, recent studies revealed a role for CoA in the redox regulation by the S-thiolation of cysteine residues in cellular proteins. The intracellular concentration and distribution in different cellular compartments of CoA and its derivatives are controlled by several extracellular stimuli such as nutrients, hormones, metabolites, and cellular stresses. Perturbations of the biosynthesis and homeostasis of CoA and/or acyl-CoA are connected with several pathological conditions, including cancer, myopathies, and cardiomyopathies. In the most recent years, defects in genes involved in CoA production and distribution have been found in patients affected by rare forms of neurodegenerative and neurodevelopmental disorders. In this review, we will summarize the most relevant aspects of CoA cellular metabolism, their role in the pathogenesis of selected neurodevelopmental and neurodegenerative disorders, and recent advancements in the search for therapeutic approaches for such diseases. Full article
(This article belongs to the Special Issue Brain Evolution, Development, and Diseases)
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16 pages, 821 KiB  
Review
The Participation of Microglia in Neurogenesis: A Review
by Diego R. Pérez-Rodríguez, Idoia Blanco-Luquin and Maite Mendioroz
Brain Sci. 2021, 11(5), 658; https://0-doi-org.brum.beds.ac.uk/10.3390/brainsci11050658 - 18 May 2021
Cited by 28 | Viewed by 3674
Abstract
Adult neurogenesis was one of the most important discoveries of the last century, helping us to better understand brain function. Researchers recently discovered that microglia play an important role in this process. However, various questions remain concerning where, at what stage, and what [...] Read more.
Adult neurogenesis was one of the most important discoveries of the last century, helping us to better understand brain function. Researchers recently discovered that microglia play an important role in this process. However, various questions remain concerning where, at what stage, and what types of microglia participate. In this review, we demonstrate that certain pools of microglia are determinant cells in different phases of the generation of new neurons. This sheds light on how cells cooperate in order to fine tune brain organization. It also provides us with a better understanding of distinct neuronal pathologies. Full article
(This article belongs to the Special Issue Brain Evolution, Development, and Diseases)
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20 pages, 2833 KiB  
Review
Preconditioning Strategies to Enhance Neural Stem Cell-Based Therapy for Ischemic Stroke
by Farah Amna Othman and Suat Cheng Tan
Brain Sci. 2020, 10(11), 893; https://0-doi-org.brum.beds.ac.uk/10.3390/brainsci10110893 - 23 Nov 2020
Cited by 25 | Viewed by 3705
Abstract
Transplantation of neural stem cells (NSCs) has been proposed as an alternative novel therapy to replace damaged neural circuitry after ischemic stroke onset. Nonetheless, albeit the potential of these cells for stroke therapy, many critical challenges are yet to be overcome to reach [...] Read more.
Transplantation of neural stem cells (NSCs) has been proposed as an alternative novel therapy to replace damaged neural circuitry after ischemic stroke onset. Nonetheless, albeit the potential of these cells for stroke therapy, many critical challenges are yet to be overcome to reach clinical applications. The major limitation of the NSC-based therapy is its inability to retain most of the donor stem cells after grafting into an ischemic brain area which is lacking of essential oxygen and nutrients for the survival of transplanted cells. Low cell survival rate limits the capacity of NSCs to repair the injured area and this poses a much more difficult challenge to the NSC-based therapy for ischemic stroke. In order to enhance the survival of transplanted cells, several stem cell culture preconditioning strategies have been employed. For ischemic diseases, hypoxic preconditioning is the most commonly applied strategy since the last few decades. Now, the preconditioning strategies have been developed and expanded enormously throughout years of efforts. This review systematically presented studies searched from PubMed, ScienceDirect, Web of Science, Scopus and the Google Scholar database up to 31 March 2020 based on search words containing the following terms: “precondition” or “pretreatment” and “neural stem cell” and “ischemic stroke”. The searched data comprehensively reported seven major NSC preconditioning strategies including hypoxic condition, small drug molecules such as minocycline, doxycycline, interleukin-6, adjudin, sodium butyrate and nicorandil, as well as electrical stimulation using conductive polymer for ischemic stroke treatment. We discussed therapeutic benefits gained from these preconditioned NSC for in vitro and in vivo stroke studies and the detailed insights of the mechanisms underlying these preconditioning approaches. Nonetheless, we noticed that there was a scarcity of evidence on the efficacy of these preconditioned NSCs in human clinical studies, therefore, it is still too early to draw a definitive conclusion on the efficacy and safety of this active compound for patient usage. Thus, we suggest for more in-depth clinical investigations of this cell-based therapy to develop into more conscientious and judicious evidence-based therapy for clinical application in the future. Full article
(This article belongs to the Special Issue Brain Evolution, Development, and Diseases)
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Other

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4 pages, 620 KiB  
Comment
The Implementation of Preconditioned Epidermal Neural Crest Stem Cells to Combat Ischemic Stroke. Comment on Othman, F.A.; Tan, S.C. Preconditioning Strategies to Enhance Neural Stem Cell-Based Therapy for Ischemic Stroke. Brain Sci. 2020, 10, 893
by Sareh Pandamooz, Benjamin Jurek, Mohammad Saied Salehi, Mandana Mostaghel, Jaleel A. Miyan, Mehdi Dianatpour and Afshin Borhani-Haghighi
Brain Sci. 2021, 11(5), 653; https://0-doi-org.brum.beds.ac.uk/10.3390/brainsci11050653 - 17 May 2021
Cited by 3 | Viewed by 2245
Abstract
In the recent review published in Brain Sciences, Othman and Tan suggested several preconditioning strategies to improve stem cell therapy after ischemic brain injury [...] Full article
(This article belongs to the Special Issue Brain Evolution, Development, and Diseases)
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9 pages, 265 KiB  
Opinion
An Interesting Molecule: γ-Aminobutyric Acid. What Can We Learn from Hydra Polyps?
by Paola Pierobon
Brain Sci. 2021, 11(4), 437; https://0-doi-org.brum.beds.ac.uk/10.3390/brainsci11040437 - 29 Mar 2021
Cited by 4 | Viewed by 2082
Abstract
Neuronal excitability is controlled primarily by γ-aminobutyric acid (GABA) in the central and peripheral nervous systems of vertebrate as well as invertebrate organisms. Besides its recognized neurotransmitter functions, GABA also plays a fundamental role in neurogenesis and synaptogenesis during embryonic development. In addition, [...] Read more.
Neuronal excitability is controlled primarily by γ-aminobutyric acid (GABA) in the central and peripheral nervous systems of vertebrate as well as invertebrate organisms. Besides its recognized neurotransmitter functions, GABA also plays a fundamental role in neurogenesis and synaptogenesis during embryonic development. In addition, GABAergic mechanisms are also involved in disorders of various peripheral tissues, ranging from diabetes to hypothyroidism to inflammatory responses. The discovery of the molecule and the history of its biosynthetic pathways in vertebrate and invertebrate phyla are summarized here. The occurrence and distribution of GABA, GABA-synthesizing enzymes, and receptors to GABA in the freshwater polyp Hydra vulgaris (Cnidaria: Hydrozoa), endowed with an early evolved nervous system, are discussed in relation to possible interactions with the microbiota, a stable component of Hydra polyps; their contribution to the evolution of nervous systems through microbe–neuronal interactions is proposed. Full article
(This article belongs to the Special Issue Brain Evolution, Development, and Diseases)
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