227 results match your criteria Advances in neurobiology[Journal]


Not Cure But Heal: Music and Medicine.

Adv Neurobiol 2018 ;21:283-307

Department of Psychology, Goldsmiths, University of London, London, UK.

Do you know that our soul is composed of harmony? Leonardo Da Vinci Despite evidence for music-specific mechanisms at the level of pitch-pattern representations, the most fascinating aspect of music is its transmodality. Recent psychological and neuroscientific evidence suggest that music is unique in the coupling of perception, cognition, action and emotion. This potentially explains why music has been since time immemorial almost inextricably linked to healing processes and should continue to be. Read More

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http://dx.doi.org/10.1007/978-3-319-94593-4_11DOI Listing
January 2018

Using Systems Biology and Mathematical Modeling Approaches in the Discovery of Therapeutic Targets for Spinal Muscular Atrophy.

Adv Neurobiol 2018 ;21:267-281

Center for Applied Clinical Genomics, Nemours Biomedical Research, Nemours/Alfred I. duPont Hospital for Children, Wilmington, DE, USA.

Systems biology uses a combination of experimental and mathematical approaches to investigate the complex and dynamic interactions with a given system or biological process. Systems biology integrates genetics, signal transduction, biochemistry and cell biology with mathematical modeling. It can be used to identify novel pathways implicated in diseases as well as to understand the mechanisms by which a specific gene is regulated. Read More

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http://link.springer.com/10.1007/978-3-319-94593-4_10
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http://dx.doi.org/10.1007/978-3-319-94593-4_10DOI Listing
January 2018
3 Reads

Large De Novo Microdeletion in Epilepsy with Intellectual and Developmental Disabilities, with a Systems Biology Analysis.

Adv Neurobiol 2018 ;21:247-266

Department of Pediatrics, Peking University First Hospital, Peking University Health Science Center, Beijing, China.

Epilepsy is one of the most common complex neurological diseases. It is frequently associated with intellectual and developmental disabilities (ID/DD). In recent years, copy number variation (CNV), especially microdeletion, was proven to be a potential key factor of genetic epilepsy. Read More

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http://link.springer.com/10.1007/978-3-319-94593-4_9
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http://dx.doi.org/10.1007/978-3-319-94593-4_9DOI Listing
January 2018
17 Reads

Synaptic Plasticity and Synchrony in the Anterior Cingulate Cortex Circuitry: A Neural Network Approach to Causality of Chronic Visceral Pain and Associated Cognitive Deficits.

Authors:
Ying Li

Adv Neurobiol 2018 ;21:219-245

Department of Biomedical Sciences, City University of Hong Kong, Kowloon, Hong Kong.

Human brain imaging studies have demonstrated the importance of cortical neuronal networks in the perception of pain in patients with functional bowel disease such as irritable bowel syndrome (IBS).Studies have identified an enhanced response in the anterior cingulate cortex (ACC) to colorectal distension in viscerally hypersensitive (VH) rats. Electrophysiological recordings show long-lasting potentiation of local field potential (LFP) in the medial thalamus (MT)-ACC synapses in VH rats. Read More

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http://link.springer.com/10.1007/978-3-319-94593-4_8
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http://dx.doi.org/10.1007/978-3-319-94593-4_8DOI Listing
January 2018
25 Reads

Genome-Scale Brain Metabolic Networks as Scaffolds for the Systems Biology of Neurodegenerative Diseases: Mapping Metabolic Alterations.

Adv Neurobiol 2018 ;21:195-217

Department of Bioengineering, Gebze Technical University, Gebze, Kocaeli, Turkey.

Systems-based investigation of diseases requires integrated analysis of cellular networks and high-throughput data of gene products. The use of genome-scale metabolic networks for such integration has led to the elucidation of cellular mechanisms for several cell types from microorganisms to plants. It has become easier and cheaper to generate high-throughput data over years in the form of transcriptome, proteome and metabolome. Read More

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http://dx.doi.org/10.1007/978-3-319-94593-4_7DOI Listing
January 2018
3 Reads

Mapping Molecular Datasets Back to the Brain Regions They are Extracted from: Remembering the Native Countries of Hypothalamic Expatriates and Refugees.

Adv Neurobiol 2018 ;21:101-193

VA Puget Sound Health Care System, Office of Research and Development Medical Research Service, Department of Veterans Affairs Medical Center, Seattle, WA, USA.

This article focuses on approaches to link transcriptomic, proteomic, and peptidomic datasets mined from brain tissue to the original locations within the brain that they are derived from using digital atlas mapping techniques. We use, as an example, the transcriptomic, proteomic and peptidomic analyses conducted in the mammalian hypothalamus. Following a brief historical overview, we highlight studies that have mined biochemical and molecular information from the hypothalamus and then lay out a strategy for how these data can be linked spatially to the mapped locations in a canonical brain atlas where the data come from, thereby allowing researchers to integrate these data with other datasets across multiple scales. Read More

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http://dx.doi.org/10.1007/978-3-319-94593-4_6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6310046PMC
January 2018

Synaptic Excitatory-Inhibitory Balance Underlying Efficient Neural Coding.

Adv Neurobiol 2018 ;21:85-100

State Key Laboratory of Medical Neurobiology, School of Life Science and Human Phenome Institute, Institutes of Brain Science, Institute of Science and Technology for Brain-Inspired Intelligence, Fudan University, Shanghai, China.

Both theoretical and experimental evidence indicate that synaptic excitation and inhibition in the cerebral cortex are well-balanced during the resting state and sensory processing. Here, we briefly summarize the evidence for how neural circuits are adjusted to achieve this balance. Then, we discuss how such excitatory and inhibitory balance shapes stimulus representation and information propagation, two basic functions of neural coding. Read More

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http://link.springer.com/10.1007/978-3-319-94593-4_5
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http://dx.doi.org/10.1007/978-3-319-94593-4_5DOI Listing
January 2018
12 Reads

Context-Dependent Adjustments in Executive Control of Goal-Directed Behaviour: Contribution of Frontal Brain Areas to Conflict-Induced Behavioural Adjustments in Primates.

Adv Neurobiol 2018 ;21:71-83

Department of Experimental Psychology, Oxford University, Oxford, UK.

Psychophysical studies in humans indicate that the performance in various tasks is affected by contextual factors such as conflict level and error commission. It is generally believed that contextual factors influence the executive control processes and consequently modulate ongoing behaviour. Imaging studies suggest that dorsolateral prefrontal cortex and anterior cingulate cortex play crucial roles in mediating these context-dependent adjustments in executive control of behaviour. Read More

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http://dx.doi.org/10.1007/978-3-319-94593-4_4DOI Listing
January 2018
2 Reads

The Hippocampal Ensemble Code for Spatial Navigation and Episodic Memory.

Authors:
Susumu Takahashi

Adv Neurobiol 2018 ;21:49-70

Graduate School of Brain Science, Doshisha University, Kyoto, Japan.

In our minds we can vividly re-experience a series of past events or episodes that occurred along space and time. In 1957, a highly influential clinical investigation published by Scoville and Milner suggested that episodic memory retrieval is severely impaired after physical damage occurs to the hippocampus. In fact, loss of the hippocampus can lead to a profound disturbance to spatial navigation. Read More

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http://dx.doi.org/10.1007/978-3-319-94593-4_3DOI Listing
January 2018
4 Reads

Neural Circuits Mediating Fear Learning and Extinction.

Adv Neurobiol 2018 ;21:35-48

Queensland Brain Institute, The University of Queensland, Brisbane, QLD, Australia.

The activity of neural circuits that underpin particular behaviours are one of the most interesting questions in neurobiology today. This understanding will not only lead to a detailed understanding of learning and memory formation, but also provides a platform for the development of novel therapeutic approaches to a range of neurological disorders that afflict humans. Among the different behavioural paradigms, Pavlovian fear conditioning and its extinction are two of the most extensively used to study acquisition, consolidation and retrieval of fear-related memories. Read More

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http://link.springer.com/10.1007/978-3-319-94593-4_2
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http://dx.doi.org/10.1007/978-3-319-94593-4_2DOI Listing
January 2018
30 Reads

Neuronal Bases of Systemic Organization of Behavior.

Adv Neurobiol 2018 ;21:1-33

Shvyrkov's Lab, Neural Bases of Mind, Institute of Psychology, Russian Academy of Sciences, Moscow, Russia.

Despite the years of studies in the field of systems neuroscience, functions of neural circuits and behavior-related systems are still not entirely clear. The systems description of brain activity has recently been associated with cognitive concepts, e.g. Read More

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http://link.springer.com/10.1007/978-3-319-94593-4_1
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http://dx.doi.org/10.1007/978-3-319-94593-4_1DOI Listing
January 2018
13 Reads

Lost in Translation: Evidence for Protein Synthesis Deficits in ALS/FTD and Related Neurodegenerative Diseases.

Adv Neurobiol 2018 ;20:283-301

Department of Molecular and Cellular Biology, University of Arizona, Tucson, AZ, USA.

Cells utilize a complex network of proteins to regulate translation, involving post-transcriptional processing of RNA and assembly of the ribosomal unit. Although the complexity provides robust regulation of proteostasis, it also offers several opportunities for translational dysregulation, as has been observed in many neurodegenerative disorders. Defective mRNA localization, mRNA sequatration, inhibited ribogenesis, mutant tRNA synthetases, and translation of hexanucleotide expansions have all been associated with neurodegenerative disease. Read More

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http://dx.doi.org/10.1007/978-3-319-89689-2_11DOI Listing
October 2018
10 Reads

Senataxin, A Novel Helicase at the Interface of RNA Transcriptome Regulation and Neurobiology: From Normal Function to Pathological Roles in Motor Neuron Disease and Cerebellar Degeneration.

Adv Neurobiol 2018 ;20:265-281

Department of Neurology, Duke University School of Medicine, Durham, NC, USA.

Senataxin (SETX) is a DNA-RNA helicase whose C-terminal region shows homology to the helicase domain of the yeast protein Sen1p. Genetic discoveries have established the importance of SETX for neural function, as recessive mutations in the SETX gene cause Ataxia with Oculomotor Apraxia type 2 (AOA2) (OMIM: 606002), which is the third most common form of recessive ataxia, after Friedreich's ataxia and Ataxia-Telangiectasia. In addition, rare, dominant SETX mutations cause a juvenile-onset form of Amyotrophic Lateral Sclerosis (ALS), known as ALS4. Read More

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http://link.springer.com/10.1007/978-3-319-89689-2_10
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October 2018
11 Reads

Mechanisms Associated with TDP-43 Neurotoxicity in ALS/FTLD.

Adv Neurobiol 2018 ;20:239-263

Tanz Centre for Research in Neurodegenerative Diseases and Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, M5T 2S8, Canada.

The discovery of TDP-43 as a major disease protein in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) was first made in 2006. Prior to 2006 there were only 11 publications related to TDP-43, now there are over 2000, indicating the importance of TDP-43 to unraveling the complex molecular mechanisms that underpin the pathogenesis of ALS/FTLD. Subsequent to this discovery, TDP-43 pathology was also found in other neurodegenerative diseases, including Alzheimer's disease, the significance of which is still in the early stages of exploration. Read More

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http://link.springer.com/10.1007/978-3-319-89689-2_9
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http://dx.doi.org/10.1007/978-3-319-89689-2_9DOI Listing
October 2018
5 Reads

Deregulation of RNA Metabolism in Microsatellite Expansion Diseases.

Adv Neurobiol 2018 ;20:213-238

Department of Biochemistry, University of Illinois, Urbana-Champaign, IL, USA.

RNA metabolism impacts different steps of mRNA life cycle including splicing, polyadenylation, nucleo-cytoplasmic export, translation, and decay. Growing evidence indicates that defects in any of these steps lead to devastating diseases in humans. This chapter reviews the various RNA metabolic mechanisms that are disrupted in Myotonic Dystrophy-a trinucleotide repeat expansion disease-due to dysregulation of RNA-Binding Proteins. Read More

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http://dx.doi.org/10.1007/978-3-319-89689-2_8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6323645PMC
October 2018
20 Reads

Stress Granules and ALS: A Case of Causation or Correlation?

Adv Neurobiol 2018 ;20:173-212

Department of Molecular and Cellular Biology, University of Arizona, Tucson, AZ, USA.

Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disease characterized by cytoplasmic protein aggregates within motor neurons. These aggregates are linked to ALS pathogenesis. Recent evidence has suggested that stress granules may aid the formation of ALS protein aggregates. Read More

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http://dx.doi.org/10.1007/978-3-319-89689-2_7DOI Listing
October 2018

RNP Assembly Defects in Spinal Muscular Atrophy.

Adv Neurobiol 2018 ;20:143-171

Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.

Spinal muscular atrophy (SMA) is a motor neuron disease caused by mutations/deletions within the survival of motor neuron 1 (SMN1) gene that lead to a pathological reduction of SMN protein levels. SMN is part of a multiprotein complex, functioning as a molecular chaperone that facilitates the assembly of spliceosomal small nuclear ribonucleoproteins (snRNP). In addition to its role in spliceosome formation, SMN has also been found to interact with mRNA-binding proteins (mRBPs), and facilitate their assembly into mRNP transport granules. Read More

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http://dx.doi.org/10.1007/978-3-319-89689-2_6DOI Listing
October 2018
1 Read

RNA Degradation in Neurodegenerative Disease.

Adv Neurobiol 2018 ;20:103-142

Neuroscience Graduate Program and Department of Neurology, University of Michigan School of Medicine, Ann Arbor, MI, USA.

Ribonucleic acid (RNA) homeostasis is dynamically modulated in response to changing physiological conditions. Tight regulation of RNA abundance through both transcription and degradation determines the amount, timing, and location of protein translation. This balance is of particular importance in neurons, which are among the most metabolically active and morphologically complex cells in the body. Read More

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http://dx.doi.org/10.1007/978-3-319-89689-2_5DOI Listing
October 2018
1 Read

RNA Nucleocytoplasmic Transport Defects in Neurodegenerative Diseases.

Adv Neurobiol 2018 ;20:85-101

Department of Neurobiology, Barrow Neurological Institute, Phoenix, AZ, USA.

In eukaryotic cells, transcription and translation are compartmentalized by the nuclear membrane, requiring an active transport of RNA from the nucleus into the cytoplasm. This is accomplished by a variety of transport complexes that contain either a member of the exportin family of proteins and translocation fueled by GTP hydrolysis or in the case of mRNA by complexes containing the export protein NXF1. Recent evidence indicates that RNA transport is altered in a number of different neurodegenerative diseases including Huntington's disease, Alzheimer's disease, frontotemporal dementia, and amyotrophic lateral sclerosis. Read More

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http://dx.doi.org/10.1007/978-3-319-89689-2_4DOI Listing
October 2018
1 Read

RNA Editing Deficiency in Neurodegeneration.

Adv Neurobiol 2018 ;20:63-83

Department of Neurobiology and Neurology, Dignityhealth St. Joseph's Hospital, Barrow Neurological Institute, Phoenix, AZ, USA.

The molecular process of RNA editing allows changes in RNA transcripts that increase genomic diversity. These highly conserved RNA editing events are catalyzed by a group of enzymes known as adenosine deaminases acting on double-stranded RNA (ADARs). ADARs are necessary for normal development, they bind to over thousands of genes, impact millions of editing sites, and target critical components of the central nervous system (CNS) such as glutamate receptors, serotonin receptors, and potassium channels. Read More

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http://dx.doi.org/10.1007/978-3-319-89689-2_3DOI Listing
October 2018
12 Reads

Mechanism of Splicing Regulation of Spinal Muscular Atrophy Genes.

Adv Neurobiol 2018 ;20:31-61

Department of Biomedical Sciences, Iowa State University, Ames, IA, USA.

Spinal muscular atrophy (SMA) is one of the major genetic disorders associated with infant mortality. More than 90% cases of SMA result from deletions or mutations of Survival Motor Neuron 1 (SMN1) gene. SMN2, a nearly identical copy of SMN1, does not compensate for the loss of SMN1 due to predominant skipping of exon 7. Read More

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http://dx.doi.org/10.1007/978-3-319-89689-2_2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6026014PMC
October 2018
5 Reads

An Epigenetic Spin to ALS and FTD.

Adv Neurobiol 2018 ;20:1-29

Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are two devastating and lethal neurodegenerative diseases seen comorbidly in up to 15% of patients. Despite several decades of research, no effective treatment or disease-modifying strategies have been developed. We now understand more than before about the genetics and biology behind ALS and FTD, but the genetic etiology for the majority of patients is still unknown and the phenotypic variability observed across patients, even those carrying the same mutation, is enigmatic. Read More

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October 2018
6 Reads

A Unique Sub-Pocket for Improvement of Selectivity of Phosphodiesterase Inhibitors in CNS.

Adv Neurobiol 2017 ;17:463-471

Department of Biochemistry and Biophysics and Lineberger Comprehensive Cancer Center, The University of North Carolina, 120 Mason Farm Road, Chapel Hill, NC, 27599-7260, USA.

This chapter describes crystal structures of phosphodiesterases (PDEs) that are involved in CNS diseases and their interactions with family selective inhibitors. The structural comparison identifies a small hydrophobic pocket next to the active site, which may be valuable for improvement of selectivity of PDE inhibitors. Read More

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http://link.springer.com/10.1007/978-3-319-58811-7_17
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http://dx.doi.org/10.1007/978-3-319-58811-7_17DOI Listing
January 2018
5 Reads

Genetic Understanding of Stroke Treatment: Potential Role for Phosphodiesterase Inhibitors.

Adv Neurobiol 2017 ;17:445-461

Institute of Genetics and Hospital for Genetic Diseases, Osmania University, Begumpet, Hyderabad, 500016, India.

Phosphodiesterase (PDE) gene family is a large family having at least 21 genes and multiple versions (isoforms) of the phosphodiesterase enzymes. These enzymes catalyze the inactivation of intracellular mediators of signal transduction such as cAMP and cGMP and therefore, play a pivotal role in various cellular functions. PDE inhibitors (PDEI) are drugs that block one or more of the five subtypes of the PDE family and thereby prevent inactivation of the intracellular cAMP and cGMP by the respective PDE-subtypes. Read More

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http://dx.doi.org/10.1007/978-3-319-58811-7_16DOI Listing
January 2018
29 Reads

Targeting Phosphodiesterases in Pharmacotherapy for Substance Dependence.

Adv Neurobiol 2017 ;17:413-444

Department of Behavioral Medicine and Psychiatry, West Virginia University Health Sciences Center, 1 Medical Center Drive, Morgantown, WV, 26506, USA.

Substance dependence is a chronic relapsing brain disorder associated with adaptational changes in synaptic plasticity and neuronal functions. The high levels of substance consumption and relapse rate suggest more reliable medications are in need to better address the underlying causes of this disease. It has been well established that the intracellular second messengers cyclic AMP (cAMP) and cyclic GMP (cGMP) and their signaling systems play an important role in the molecular mechanisms of substance taking behaviors. Read More

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http://dx.doi.org/10.1007/978-3-319-58811-7_15DOI Listing
January 2018

PDE Inhibitors for the Treatment of Schizophrenia.

Adv Neurobiol 2017 ;17:385-409

Clinical Development, Intra-Cellular Therapies Inc (ITI), 430 East 29th Street, Suite 900, New York, NY, 10016, USA.

Schizophrenia is a pervasive neuropsychiatric disorder affecting over 1% of the world's population. Dopamine system dysfunction is strongly implicated in the etiology of schizophrenia. Data support the long-standing concept of schizophrenia as a disease characterized by hyperactivity within midbrain (striatal D2) dopamine systems. Read More

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http://dx.doi.org/10.1007/978-3-319-58811-7_14DOI Listing
January 2018
22 Reads

Phosphodiesterase 1: A Unique Drug Target for Degenerative Diseases and Cognitive Dysfunction.

Adv Neurobiol 2017 ;17:349-384

Alexandria Center for Life Science, Intra-Cellular Therapies, Inc., New York, 10016, NY, USA.

The focus of this chapter is on the cyclic nucleotide phosphodiesterase 1 (PDE1) family. PDE1 is one member of the 11 PDE families (PDE 1-11). It is the only phosphodiesterase family that is calcium/calmodulin activated. Read More

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http://link.springer.com/10.1007/978-3-319-58811-7_13
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http://dx.doi.org/10.1007/978-3-319-58811-7_13DOI Listing
January 2018
16 Reads

The Role of Phosphodiesterase-2 in Psychiatric and Neurodegenerative Disorders.

Adv Neurobiol 2017 ;17:307-347

Department of Pharmaceutical Sciences, School of Pharmacy and Pharmaceutical Sciences, University at Buffalo, The State University of New York, Buffalo, NY, 14214, USA.

Cyclic nucleotide PDEs are a super-family of enzymes responsible for regulating intracellular levels of the second messengers cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP). Through their catalysis, PDEs are able to exert tight regulation over these important intracellular signaling cascades. Previously, PDEs have been implicated in learning and memory, as well as in mood disorders, such as anxiety and depression. Read More

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http://link.springer.com/10.1007/978-3-319-58811-7_12
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http://dx.doi.org/10.1007/978-3-319-58811-7_12DOI Listing
January 2018
4 Reads

Role of Phosphodiesterases in Huntington's Disease.

Adv Neurobiol 2017 ;17:285-304

Neuroanatomy Laboratory, Santa Lucia Foundation, Rome, 06501703061, Italy.

Huntington's disease (HD) is an autosomal-dominant rare inherited neurodegenerative disease characterized by a wide variety of symptoms encompassing movement, cognition and behaviour. The cause of the disease is a genetic mutation in the huntingtin protein. The mutation leads to an unstable CAG expansion, translated into a polyglutamine domain within the disease protein. Read More

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http://dx.doi.org/10.1007/978-3-319-58811-7_11DOI Listing
January 2018
8 Reads

Regulation of Striatal Neuron Activity by Cyclic Nucleotide Signaling and Phosphodiesterase Inhibition: Implications for the Treatment of Parkinson's Disease.

Adv Neurobiol 2017 ;17:257-283

Department of Neuroscience, Rosalind Franklin University of Medicine and Science, 3333 Green Bay Road, North Chicago, IL, 60064, USA.

Cyclic nucleotide phosphodiesterase (PDE) enzymes catalyze the hydrolysis and inactivation of cyclic nucleotides (cAMP/cGMP) in the brain. Several classes of PDE enzymes with distinct tissue distributions, cyclic nucleotide selectivity, and regulatory factors are highly expressed in brain regions subserving cognitive and motor processes known to be disrupted in neurodegenerative diseases such as Parkinson's disease (PD). Furthermore, small-molecule inhibitors of several different PDE family members alter cyclic nucleotide levels and favorably enhance motor performance and cognition in animal disease models. Read More

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http://dx.doi.org/10.1007/978-3-319-58811-7_10DOI Listing
January 2018
15 Reads

Role of PDE9 in Cognition.

Adv Neurobiol 2017 ;17:231-254

Boehringer Ingelheim Pharma GmbH & Co. KG, Ingelheim am Rhein, Germany.

Inhibition of phosphodiesterases (PDEs) has been demonstrated to enhance performance of animals in various cognition tasks and accordingly PDE inhibitors have been proposed as new approach for treatment of cognitive dysfunction (Reneerkens et al. Psychopharmacology 202:419-443, 2009; Schmidt Curr Top Med Chem 10(2):222-230, 2010). One of the eleven PDE isoforms, showing expression in cognition relevant brain regions across species, is PDE9, which hydrolyzes cGMP only. Read More

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http://dx.doi.org/10.1007/978-3-319-58811-7_9DOI Listing
January 2018
1 Read

A Role for Phosphodiesterase 11A (PDE11A) in the Formation of Social Memories and the Stabilization of Mood.

Authors:
Michy P Kelly

Adv Neurobiol 2017 ;17:201-230

Department of Pharmacology, Physiology and Neuroscience, University of South Carolina School of Medicine, 6439 Garners Ferry Road, VA Bldg 1, 3rd Floor, D-12, Columbia, SC, 29209, USA.

The most recently discovered 3',5'-cyclic nucleotide phosphodiesterase family is the Phosphodiesterase 11 (PDE11) family, which is encoded by a single gene PDE11A. PDE11A is a dual-specific PDE, breaking down both cAMP and cGMP. There are four PDE11A splice variants (PDE11A1-4) with distinct tissue expression profiles and unique N-terminal regulatory regions, suggesting that each isoform could be individually targeted with a small molecule or biologic. Read More

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http://dx.doi.org/10.1007/978-3-319-58811-7_8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5652326PMC
January 2018

The Past, Present, and Future of Phosphodiesterase-4 Modulation for Age-Induced Memory Loss.

Adv Neurobiol 2017 ;17:169-199

Department of Behavioral Medicine and Psychiatry, West Virginia University Health Sciences Center, 1 Medical Center Drive, Morgantown, WV, 26506, USA.

The purpose of this chapter is to highlight the state of progress for phosphodiesterase-4 (PDE4) modulation as a potential therapeutic for psychiatric illness, and to draw attention to particular hurdles and obstacles that must be overcome in future studies to develop PDE4-mediated therapeutics. Pathological and non-pathological related memory loss will be the focus of the chapter; however, we will at times also touch upon other psychiatric illnesses like anxiety and depression. First, we will provide a brief background of PDE4, and the rationale for its extensive study in cognition. Read More

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http://dx.doi.org/10.1007/978-3-319-58811-7_7DOI Listing
January 2018
7 Reads

From Age-Related Cognitive Decline to Alzheimer's Disease: A Translational Overview of the Potential Role for Phosphodiesterases.

Adv Neurobiol 2017 ;17:135-168

Department of Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Maastricht University, PO Box 616, 6200, MD, Maastricht, The Netherlands.

Phosphodiesterase inhibitors (PDE-Is) are pharmacological compounds enhancing cAMP and/or cGMP signaling. Both these substrates affect neural communication by influencing presynaptic neurotransmitter release and postsynaptic intracellular pathways after neurotransmitter binding to its receptor. Both cAMP and cGMP play an important role in a variety of cellular functions including neuroplasticity and neuroprotection. Read More

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http://dx.doi.org/10.1007/978-3-319-58811-7_6DOI Listing
January 2018
7 Reads

Phosphodiesterase-4B as a Therapeutic Target for Cognitive Impairment and Obesity-Related Metabolic Diseases.

Adv Neurobiol 2017 ;17:103-131

School of Biomedical Sciences, University of Leeds, Leeds, LS2 9JT, UK.

People in modern, affluent societies are living longer but also becoming increasingly overweight. With increased life expectancy comes increased risk of developing age-related cognitive decline and neurodegenerative diseases, such that an increasing proportion of life may be lived with cognitive impairment as age increases. Obesity is associated with poorer cognitive function in elderly subjects, and often leads to ill-health arising from various complications such as metabolic syndrome and type-2 diabetes mellitus. Read More

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http://dx.doi.org/10.1007/978-3-319-58811-7_5DOI Listing
January 2018
15 Reads

The PDE4 cAMP-Specific Phosphodiesterases: Targets for Drugs with Antidepressant and Memory-Enhancing Action.

Authors:
Graeme B Bolger

Adv Neurobiol 2017 ;17:63-102

Departments of Medicine and Pharmacology, University of Alabama at Birmingham, 1720 2nd Avenue South, NP 2501, Birmingham, AL, 35294-3300, USA.

The PDE4 cyclic nucleotide phosphodiesterases are essential regulators of cAMP abundance in the CNS through their ability to regulate PKA activity, the phosphorylation of CREB, and other important elements of signal transduction. In pre-clinical models and in early-stage clinical trials, PDE4 inhibitors have been shown to have antidepressant and memory-enhancing activity. However, the development of clinically-useful PDE4 inhibitors for CNS disorders has been limited by variable efficacy and significant side effects. Read More

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http://dx.doi.org/10.1007/978-3-319-58811-7_4DOI Listing
January 2018
20 Reads

Interaction of Cdk5 and cAMP/PKA Signaling in the Mediation of Neuropsychiatric and Neurodegenerative Diseases.

Adv Neurobiol 2017 ;17:45-61

Department of Behavioral Medicine and Psychiatry, West Virginia University Health Sciences Center, 1 Medical Center Drive, Morgantown, WV, 26506, USA.

Both cyclin-dependent kinase 5 (Cdk5) and cyclic AMP (cAMP)/protein kinase A (PKA) regulate fundamental central nervous system (CNS) functions including neuronal survival, neurite and axonal outgrowth, neuron development and cognition. Cdk5, a serine/threonine kinase, is activated by p35 or p39 and phosphorylates multiple signaling components of various pathways, including cAMP/PKA signaling. Here, we review the recent literature on the interaction between Cdk5 and cAMP/PKA signaling and their role in the mediation of CNS functions and neuropsychiatric and neurodegenerative diseases. Read More

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http://link.springer.com/10.1007/978-3-319-58811-7_3
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http://dx.doi.org/10.1007/978-3-319-58811-7_3DOI Listing
January 2018
3 Reads

Current Understanding of PDE10A in the Modulation of Basal Ganglia Circuitry.

Adv Neurobiol 2017 ;17:15-43

AstraZeneca Neuroscience, Innovative Medicines and Early Development Biotech Unit, Waltham, MA, 02451, USA.

The basal ganglia are a forebrain network of interconnected nuclei that are involved in action selection, reward circuits and coordinating movement. PDE10A inhibition has been proposed as a novel way to modulate basal ganglia circuitry and to ameliorate symptoms in Huntington's disease, Parkinson's disease and Schizophrenia. However, despite encouraging results from pre-clinical models, PDE10A inhibitors failed to show efficacy as an antipsychotic in several clinical trials. Read More

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http://dx.doi.org/10.1007/978-3-319-58811-7_2DOI Listing
January 2018
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Phosphodiesterase Diversity and Signal Processing Within cAMP Signaling Networks.

Adv Neurobiol 2017 ;17:3-14

Departments of Pharmacology and Systems Therapeutics, Friedman Brain Institute, System Biology Center New York, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, Box 1215, New York, NY, 10029, USA.

A large number of neuromodulators activate G-protein coupled receptors (GPCRs) and mediate their cellular actions via the regulation of intracellular cAMP, the small highly diffusible second messenger. In fact, in the same neuron several different GPCRs can regulate cAMP with seemingly identical timecourses that give rise to distinct signaling outcomes, suggesting that cAMP does not have equivalent access to all its downstream effectors and may exist within defined intracellular pools or domains. cAMP compartmentalization is the process that allows the neuron to differentially interpret these various intracellular cAMP signals into cellular response. Read More

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http://dx.doi.org/10.1007/978-3-319-58811-7_1DOI Listing
January 2018
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Functional Neuroimaging in Obesity Research.

Adv Neurobiol 2017 ;19:239-248

IBILI-Institute for Biomedical Imaging and Life Sciences, Faculty of Medicine, University of Coimbra, Coimbra, Portugal.

Functional neuroimaging is beginning to yield valuable insights into the neurobiological underpinnings of the effects of obesity on neural circuits. Functional magnetic resonance imaging (fMRI), positron emission tomography (PET), and single-photon emission computed tomography (SPECT) studies have been used to identify aberrant activation patterns in regions implicated in reward (e.g. Read More

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http://dx.doi.org/10.1007/978-3-319-63260-5_10DOI Listing
November 2018
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Central Modulation of Energy Homeostasis and Cognitive Performance After Bariatric Surgery.

Authors:
Hans Eickhoff

Adv Neurobiol 2017 ;19:213-236

Institute of Physiology, Institute for Biomedical Imaging and Life Sciences-IBILI, Faculty of Medicine, University of Coimbra, Coimbra, Portugal.

In moderately or morbidly obese patients, bariatric surgery has been proven to be an effective therapeutic approach to control body weight and comorbidities. Surgery-mediated modulation of brain function via modified postoperative secretion of gut peptides and vagal nerve stimulation was identified as an underlying mechanism in weight loss and improvement of weight-related diseases. Increased basal and postprandial plasma levels of gastrointestinal hormones like glucagon-like peptide 1 and peptide YY that act on specific areas of the hypothalamus to reduce food intake, either directly or mediated by the vagus nerve, are observed after surgery while suppression of meal-induced ghrelin release is increased. Read More

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http://dx.doi.org/10.1007/978-3-319-63260-5_9DOI Listing
November 2018
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Multiple Sclerosis: Implications of Obesity in Neuroinflammation.

Adv Neurobiol 2017 ;19:191-210

Neurology Department, Centro Hospitalar e Universitário de Coimbra, Coimbra, Portugal.

Since the discovery of the remarkable properties of adipose tissue as a metabolically active organ, several evidences on the possible link between obesity and the pathogenesis of multiple sclerosis (MS) have been gathered. Obesity in early life, mainly during adolescence, has been proposed as a relevant risk factor for late MS development. Moreover, once MS is initiated, obesity can contribute to increase disease severity by negatively influencing disease progress. Read More

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http://dx.doi.org/10.1007/978-3-319-63260-5_8DOI Listing
November 2018
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Cerebrovascular Disease: Consequences of Obesity-Induced Endothelial Dysfunction.

Adv Neurobiol 2017 ;19:163-189

Institute of Physiology, Institute for Biomedical Imaging and Life Sciences-IBILI, Faculty of Medicine, University of Coimbra, Coimbra, Portugal.

Despite the well-known global impact of overweight and obesity in the incidence of cerebrovascular disease, many aspects of this association are still inconsistently defined. In this chapter we aim to present a critical review on the links between obesity and both ischemic and hemorrhagic stroke and discuss its influence on functional outcomes, survival, and current treatments to acute and chronic stroke. The role of cerebrovascular endothelial function and respective modulation is also described as well as its laboratory and clinical assessment. Read More

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http://dx.doi.org/10.1007/978-3-319-63260-5_7DOI Listing
November 2018
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The Influence of Adipose Tissue on Brain Development, Cognition, and Risk of Neurodegenerative Disorders.

Adv Neurobiol 2017 ;19:151-161

Neurology Department, Centro Hospitalar e Universitário de Coimbra, Coimbra, Portugal.

The brain is a highly metabolic organ and thus especially vulnerable to changes in peripheral metabolism, including those induced by obesity-associated adipose tissue dysfunction. In this context, it is likely that the development and maturation of neurocognitive circuits may also be affected and modulated by metabolic environmental factors, beginning in utero. It is currently recognized that maternal obesity, either pre-gestational or gestational, negatively influences fetal brain development and elevates the risk of cognitive impairment and neuropsychiatric disorders in the offspring. Read More

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http://dx.doi.org/10.1007/978-3-319-63260-5_6DOI Listing
November 2018

Diabesity and Brain Energy Metabolism: The Case of Alzheimer's Disease.

Adv Neurobiol 2017 ;19:117-150

CNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.

It is widely accepted that high calorie diets and a sedentary lifestyle sturdily influence the incidence and outcome of type 2 diabetes and obesity, which can occur simultaneously, a situation called diabesity. Tightly linked with metabolic and energy regulation, a close association between diabetes and Alzheimer's disease (AD) has been proposed. Among the common pathogenic mechanisms that underpin both conditions, insulin resistance, brain glucose hypometabolism, and metabolic dyshomeostasis appear to have a pivotal role. Read More

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http://dx.doi.org/10.1007/978-3-319-63260-5_5DOI Listing
November 2018
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Hypothalamic Dysfunction in Obesity and Metabolic Disorders.

Adv Neurobiol 2017 ;19:73-116

CNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.

The hypothalamus is the brain region responsible for the maintenance of energetic homeostasis. The regulation of this process arises from the ability of the hypothalamus to orchestrate complex physiological responses such as food intake and energy expenditure, circadian rhythm, stress response, and fertility. Metabolic alterations such as obesity can compromise these hypothalamic regulatory functions. Read More

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http://dx.doi.org/10.1007/978-3-319-63260-5_4DOI Listing
November 2018
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Neuroendocrinology of Adipose Tissue and Gut-Brain Axis.

Adv Neurobiol 2017 ;19:49-70

Institute of Physiology, Institute for Biomedical Imaging and Life Sciences-IBILI, Faculty of Medicine, University of Coimbra, Coimbra, Portugal.

Food intake and energy expenditure are closely regulated by several mechanisms which involve peripheral organs and nervous system, in order to maintain energy homeostasis.Short-term and long-term signals express the size and composition of ingested nutrients and the amount of body fat, respectively. Ingested nutrients trigger mechanical forces and gastrointestinal peptide secretion which provide signals to the brain through neuronal and endocrine pathways. Read More

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http://dx.doi.org/10.1007/978-3-319-63260-5_3DOI Listing
November 2018
22 Reads

The Role of Brain in Energy Balance.

Adv Neurobiol 2017 ;19:33-48

Institute of Physiology, Institute for Biomedical Imaging and Life Sciences-IBILI, Faculty of Medicine, University of Coimbra, Coimbra, Portugal.

Energy homeostasis is regulated by homeostatic and nonhomeostatic reward circuits which are closely integrated and interrelated. Before, during, and after meals, peripheral nutritional signals, through hormonal and neuronal pathways, are conveyed to selective brain areas, namely the hypothalamic nuclei and the brainstem, the main brain areas for energy balance regulation. These orexigenic and anorexigenic centers are held responsible for the integration of those signals and for an adequate output to peripheral organs involved in metabolism and energy homeostasis. Read More

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http://dx.doi.org/10.1007/978-3-319-63260-5_2DOI Listing
November 2018
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Function and Dysfunction of Adipose Tissue.

Adv Neurobiol 2017 ;19:3-31

Institute of Physiology, Institute for Biomedical Imaging and Life Sciences-IBILI, Faculty of Medicine, University of Coimbra, Coimbra, Portugal.

Adipose tissue is an endocrine organ which is responsible for postprandial uptake of glucose and fatty acids, consequently producing a broad range of adipokines controlling several physiological functions like appetite, insulin sensitivity and secretion, immunity, coagulation, and vascular tone, among others. Many aspects of adipose tissue pathophysiology in metabolic diseases have been described in the last years. Recent data suggest two main factors for adipose tissue dysfunction: accumulation of nonesterified fatty acids and their secondary products and hypoxia. Read More

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http://dx.doi.org/10.1007/978-3-319-63260-5_1DOI Listing
November 2018
24 Reads

Erratum.

Adv Neurobiol 2017 ;15:E1

Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

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http://dx.doi.org/10.1007/978-3-319-57193-5_21DOI Listing
January 2017
1 Read