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Brain Sciences
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Neurodegeneration in Developmental and Neoplastic Disorders of the Nervous System
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Neurodegeneration in Developmental and Neoplastic Disorders of the Nervous System

A special issue of Brain Sciences (ISSN 2076-3425).

Deadline for manuscript submissions: closed (30 June 2016) | Viewed by 38915

Special Issue Editor

Dr. Basavaraj S. Balapal

E-Mail Website
Guest Editor
1. Department of Psychiatry, New York University Langone Medical Center, New York, NY, USA
2. Faculty at Columbia University Medical Center, Scientist, Center for Dementia Research, Nathan Kline Institute for Psychiatric Research, Orangeburg, New York, NY, USA
Interests: endocannabinoids; synaptic plasticity; FASD; AUD; neurodegeneration; learning and memory; epigenetics; gene expression; behavior
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The mechanisms which direct the important stages of brain development to orchestrate functional synaptic structure are gradually being elucidated. However, the mechanisms that regulate synaptic stability and neuronal loss that result in lifelong neurobehavioral outcome are not well known. Synapse loss is an early and invariant characteristic of many neurodegenerative diseases and in many cases the level of synapse loss correlates with the severity of the disease. The gestational and postnatal developments are appearing to be particularly vital for making stable neuronal connections that shape a lifetime of experience. The influence of environmental factors including drugs of abuse, exposure to toxicants, diet, and stress during gestation or early to late postnatal development have the ability to alter brain development and synaptic plasticity, resulting in lifelong intellectual disability and cognitive deficits. Hence, understanding the neurobehavioral mechanisms that underlie neurodegeneration and synaptic plasticity is crucial to understand the potential targets that will allow the development of therapies to protect synapses and improve neurobehavioral outcome.

The current Special Issue is aimed to collect a selected number of articles that demonstrate deeper insight in these topics, which bring both sound scientific and public health impacts.

Dr. Balapal S. Basavarajappa
Guest 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. 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

  • Drugs of abuse
  • Environmental toxicants
  • Alcohol
  • Epigenetics
  • Molecular mechanisms
  • Early brain development
  • Synaptic plasticity
  • Intellectual disability
  • Cognitive deficits
  • Learning and memory

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Published Papers (6 papers)

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Research

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3708 KiB  
Article
Prenatal Alcohol Exposure Affects Progenitor Cell Numbers in Olfactory Bulbs and Dentate Gyrus of Vervet Monkeys
by Mark W. Burke, Alexey Inyatkin, Maurice Ptito, Frank R. Ervin and Roberta M. Palmour
Brain Sci. 2016, 6(4), 52; https://doi.org/10.3390/brainsci6040052 - 27 Oct 2016
Cited by 7 | Viewed by 5614
Abstract
Fetal alcohol exposure (FAE) alters hippocampal cell numbers in rodents and primates, and this may be due, in part, to a reduction in the number or migration of neuronal progenitor cells. The olfactory bulb exhibits substantial postnatal cellular proliferation and a rapid turnover [...] Read more.
Fetal alcohol exposure (FAE) alters hippocampal cell numbers in rodents and primates, and this may be due, in part, to a reduction in the number or migration of neuronal progenitor cells. The olfactory bulb exhibits substantial postnatal cellular proliferation and a rapid turnover of newly formed cells in the rostral migratory pathway, while production and migration of postnatal neurons into the dentate gyrus may be more complex. The relatively small size of the olfactory bulb, compared to the hippocampus, potentially makes this structure ideal for a rapid analysis. This study used the St. Kitts vervet monkey (Chlorocebus sabeus) to (1) investigate the normal developmental sequence of post-natal proliferation in the olfactory bulb and dentate gyrus and (2) determine the effects of naturalistic prenatal ethanol exposure on proliferation at three different ages (neonate, five months and two years). Using design-based stereology, we found an age-related decrease of actively proliferating cells in the olfactory bulb and dentate gyrus for both control and FAE groups. Furthermore, at the neonatal time point, the FAE group had fewer actively proliferating cells as compared to the control group. These data are unique with respect to fetal ethanol effects on progenitor proliferation in the primate brain and suggest that the olfactory bulb may be a useful structure for studies of cellular proliferation. Full article
(This article belongs to the Special Issue Neurodegeneration in Developmental and Neoplastic Disorders of the Nervous System)
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768 KiB  
Article
Prenatal Ethanol Exposure and Whisker Clipping Disrupt Ultrasonic Vocalizations and Play Behavior in Adolescent Rats
by Jaylyn Waddell, Tianqi Yang, Eric Ho, Kristen A. Wellmann and Sandra M. Mooney
Brain Sci. 2016, 6(4), 43; https://doi.org/10.3390/brainsci6040043 - 28 Sep 2016
Cited by 10 | Viewed by 5157
Abstract
Prenatal ethanol exposure can result in social deficits in humans and animals, including altered social interaction and poor communication. Rats exposed to ethanol prenatally show reduced play fighting, and a combination of prenatal ethanol exposure and neonatal whisker clipping further reduces play fighting [...] Read more.
Prenatal ethanol exposure can result in social deficits in humans and animals, including altered social interaction and poor communication. Rats exposed to ethanol prenatally show reduced play fighting, and a combination of prenatal ethanol exposure and neonatal whisker clipping further reduces play fighting compared with ethanol exposure alone. In this study, we explored whether expression of hedonic ultrasonic vocalizations (USVs) correlated with the number of playful attacks by ethanol-exposed rats, rats subjected to postnatal sensory deprivation by whisker clipping or both compared to control animals. In normally developing rats, hedonic USVs precede such interactions and correlate with the number of play interactions exhibited in dyads. Pregnant Long-Evans rats were fed an ethanol-containing liquid diet or a control diet. After birth, male and female pups from each litter were randomly assigned to the whisker-clipped or non-whisker-clipped condition. Animals underwent a social interaction test with a normally developing play partner during early or late-adolescence. USVs were recorded during play. Prenatal ethanol exposure reduced both play and hedonic USVs in early adolescence compared to control rats and persistently reduced social play. Interestingly, ethanol exposure, whisker clipping and the combination abolished the significant correlation between hedonic USVs and social play detected in control rats in early adolescence. This relationship remained disrupted in late adolescence only in rats subjected to both prenatal ethanol and whisker clipping. Thus, both insults more persistently disrupted the relationship between social communication and social play. Full article
(This article belongs to the Special Issue Neurodegeneration in Developmental and Neoplastic Disorders of the Nervous System)
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Review

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225 KiB  
Review
From Drug-Induced Developmental Neuroapoptosis to Pediatric Anesthetic Neurotoxicity—Where Are We Now?
by Catherine E. Creeley
Brain Sci. 2016, 6(3), 32; https://doi.org/10.3390/brainsci6030032 - 16 Aug 2016
Cited by 29 | Viewed by 6290
Abstract
The fetal and neonatal periods are critical and sensitive periods for neurodevelopment, and involve rapid brain growth in addition to natural programmed cell death (i.e., apoptosis) and synaptic pruning. Apoptosis is an important process for neurodevelopment, preventing redundant, faulty, or unused neurons from [...] Read more.
The fetal and neonatal periods are critical and sensitive periods for neurodevelopment, and involve rapid brain growth in addition to natural programmed cell death (i.e., apoptosis) and synaptic pruning. Apoptosis is an important process for neurodevelopment, preventing redundant, faulty, or unused neurons from cluttering the developing brain. However, animal studies have shown massive neuronal cell death by apoptosis can also be caused by exposure to several classes of drugs, namely gamma-aminobutyric acid (GABA) agonists and N-methyl-d-aspartate (NMDA) antagonists that are commonly used in pediatric anesthesia. This form of neurotoxic insult could cause a major disruption in brain development with the potential to permanently shape behavior and cognitive ability. Evidence does suggest that psychoactive drugs alter neurodevelopment and synaptic plasticity in the animal brain, which, in the human brain, may translate to permanent neurodevelopmental changes associated with long-term intellectual disability. This paper reviews the seminal animal research on drug-induced developmental apoptosis and the subsequent clinical studies that have been conducted thus far. In humans, there is growing evidence that suggests anesthetics have the potential to harm the developing brain, but the long-term outcome is not definitive and causality has not been determined. The consensus is that there is more work to be done using both animal models and human clinical studies. Full article
(This article belongs to the Special Issue Neurodegeneration in Developmental and Neoplastic Disorders of the Nervous System)
2283 KiB  
Review
Ethanol-Induced Neurodegeneration and Glial Activation in the Developing Brain
by Mariko Saito, Goutam Chakraborty, Maria Hui, Kurt Masiello and Mitsuo Saito
Brain Sci. 2016, 6(3), 31; https://doi.org/10.3390/brainsci6030031 - 16 Aug 2016
Cited by 58 | Viewed by 9141
Abstract
Ethanol induces neurodegeneration in the developing brain, which may partially explain the long-lasting adverse effects of prenatal ethanol exposure in fetal alcohol spectrum disorders (FASD). While animal models of FASD show that ethanol-induced neurodegeneration is associated with glial activation, the relationship between glial [...] Read more.
Ethanol induces neurodegeneration in the developing brain, which may partially explain the long-lasting adverse effects of prenatal ethanol exposure in fetal alcohol spectrum disorders (FASD). While animal models of FASD show that ethanol-induced neurodegeneration is associated with glial activation, the relationship between glial activation and neurodegeneration has not been clarified. This review focuses on the roles of activated microglia and astrocytes in neurodegeneration triggered by ethanol in rodents during the early postnatal period (equivalent to the third trimester of human pregnancy). Previous literature indicates that acute binge-like ethanol exposure in postnatal day 7 (P7) mice induces apoptotic neurodegeneration, transient activation of microglia resulting in phagocytosis of degenerating neurons, and a prolonged increase in glial fibrillary acidic protein-positive astrocytes. In our present study, systemic administration of a moderate dose of lipopolysaccharides, which causes glial activation, attenuates ethanol-induced neurodegeneration. These studies suggest that activation of microglia and astrocytes by acute ethanol in the neonatal brain may provide neuroprotection. However, repeated or chronic ethanol can induce significant proinflammatory glial reaction and neurotoxicity. Further studies are necessary to elucidate whether acute or sustained glial activation caused by ethanol exposure in the developing brain can affect long-lasting cellular and behavioral abnormalities observed in the adult brain. Full article
(This article belongs to the Special Issue Neurodegeneration in Developmental and Neoplastic Disorders of the Nervous System)
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468 KiB  
Review
Maternal Malnutrition in the Etiopathogenesis of Psychiatric Diseases: Role of Polyunsaturated Fatty Acids
by Maria Grazia Morgese and Luigia Trabace
Brain Sci. 2016, 6(3), 24; https://doi.org/10.3390/brainsci6030024 - 27 Jul 2016
Cited by 26 | Viewed by 6460
Abstract
Evidence from human studies indicates that maternal metabolic state and malnutrition dramatically influence the risk for developing psychiatric complications in later adulthood. In this regard, the central role of polyunsaturated fatty acids (PUFAs), and particularly n-3 PUFAs, is emerging considering that epidemiological [...] Read more.
Evidence from human studies indicates that maternal metabolic state and malnutrition dramatically influence the risk for developing psychiatric complications in later adulthood. In this regard, the central role of polyunsaturated fatty acids (PUFAs), and particularly n-3 PUFAs, is emerging considering that epidemiological evidences have established a negative correlation between n-3 PUFA consumption and development of mood disorders. These findings were supported by clinical studies indicating that low content of n-3 PUFAs in diet is linked to an increased susceptibility to psychiatric disorders. PUFAs regulate membrane fluidity and exert their central action by modulating synaptogenesis and neurotrophic factor expression, neurogenesis, and neurotransmission. Moreover, they are precursors of molecules implicated in modulating immune and inflammatory processes in the brain. Importantly, their tissue concentrations are closely related to diet intake, especially to maternal consumption during embryonal life, considering that their synthesis from essential precursors has been shown to be inefficient in mammals. The scope of this review is to highlight the possible mechanisms of PUFA functions in the brain during pre- and post-natal period and to evaluate their role in the pathogenesis of psychiatric diseases. Full article
(This article belongs to the Special Issue Neurodegeneration in Developmental and Neoplastic Disorders of the Nervous System)
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1557 KiB  
Review
Propofol-Induced Neurotoxicity in the Fetal Animal Brain and Developments in Modifying These Effects—An Updated Review of Propofol Fetal Exposure in Laboratory Animal Studies
by Ming Xiong, Li Zhang, Jing Li, Jean Eloy, Jiang Hong Ye and Alex Bekker
Brain Sci. 2016, 6(2), 11; https://doi.org/10.3390/brainsci6020011 - 28 Mar 2016
Cited by 15 | Viewed by 5428
Abstract
In the past twenty years, evidence of neurotoxicity in the developing brain in animal studies from exposure to several general anesthetics has been accumulating. Propofol, a commonly used general anesthetic medication, administered during synaptogenesis, may trigger widespread apoptotic neurodegeneration in the developing brain [...] Read more.
In the past twenty years, evidence of neurotoxicity in the developing brain in animal studies from exposure to several general anesthetics has been accumulating. Propofol, a commonly used general anesthetic medication, administered during synaptogenesis, may trigger widespread apoptotic neurodegeneration in the developing brain and long-term neurobehavioral disturbances in both rodents and non-human primates. Despite the growing evidence of the potential neurotoxicity of different anesthetic agents in animal studies, there is no concrete evidence that humans may be similarly affected. However, given the growing evidence of the neurotoxic effects of anesthetics in laboratory studies, it is prudent to further investigate the mechanisms causing these effects and potential ways to mitigate them. Here, we review multiple studies that investigate the effects of in utero propofol exposure and the developmental agents that may modify these deleterious effects. Full article
(This article belongs to the Special Issue Neurodegeneration in Developmental and Neoplastic Disorders of the Nervous System)
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