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Essential Pathways and Circuits of Autism Pathogenesis

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889199051 Year: Pages: 181 DOI: 10.3389/978-2-88919-905-1 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Neurology --- Genetics
Added to DOAB on : 2016-01-19 14:05:46
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The Centers for Disease Control and Prevention estimate that 1 in 68 children in the United states is afflicted with autism spectrum disorders (ASD), yet at this time, there is no cure for the disease. Autism is characterized by delays in the development of many basic skills, most notably the ability to socialize and adapt to novelty. The condition is typically identified in children around 3 years of age, however the high heritability of autism suggests that the disease process begins at conception. The identification of over 500 ASD risk genes, has enabled the molecular genetic dissection of the pathogenesis of the disease in model organisms such as mice. Despite the genetic heterogeneity of ASD etiology, converging evidence suggests that these disparate genetic lesions may result in the disruption of a limited number of key biochemical pathways or circuits. Classification of patients into groups by pathogenic rather than etiological categories, will likely aid future therapeutic development and clinical trials. In this set of papers, we explore the existing evidence supporting this view. Specifically, we focus on biochemical cascades such as mTOR and ERK signaling, the mRNA network bound by FMRP and UBE3A, dorsal and ventral striatal circuits, cerebellar circuits, hypothalamic projections, as well as prefrontal and anterior cingulate cortical circuits. Special attention will be given to studies that demonstrate the necessity and/or sufficiency of genetic disruptions (e.g. by molecular deletion and/or replacement) in these pathways and circuits for producing characteristic behavioral features of autism. Necessarily these papers will be heavily weighted towards basic mechanisms elucidated in animal models, but may also include investigations in patients.

Neuronal and Psychological Underpinnings of Pathological Gambling

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889193202 Year: Pages: 132 DOI: 10.3389/978-2-88919-320-2 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2016-02-05 17:24:33
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Like in the case of drugs, gambling hijacks reward circuits in a brain which is not prepared to receive such intense stimulation. Dopamine is normally released in response to reward and uncertainty in order to allow animals to stay alive in their environment – where rewards are relatively unpredictable. In this case, behavior is regulated by environmental feedbacks, leading animals to persevere or to give up. In contrast, drugs provide a direct, intense pharmacological stimulation of the dopamine system that operates independently of environmental feedbacks, and hence causes “motivational runaways”. With respect to gambling, the confined environment experienced by gamblers favors the emergence of excitatory conditioned cues, so that positive feedbacks take over negative feedbacks. Although drugs and gambling may act differently, their abnormal activation of reward circuitry generates an underestimation of negative consequences and promotes the development of addictive/compulsive behavior. In Parkinson’s and Huntington’s disease, dopamine-related therapies may disrupt these feedbacks on dopamine signalling, potentially leading to various addictions, including pathological gambling. The goal of this Research Topic is to further our understanding of the neurobiological mechanisms underlying the development of pathological gambling. This eBook contains a cross-disciplinary collection of research and review articles, ranging in scope from animal behavioral models to human imaging studies.

Parkinson's Disease Cell Vulnerability and Disease Progression

Authors: --- ---
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889196760 Year: Pages: 194 DOI: 10.3389/978-2-88919-676-0 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2016-04-07 11:22:02
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Parkinson's disease is a neurodegenerative disorder that affects 1.5% of the global population over 65 years of age. The hallmark feature of this disease is the degeneration of dopamine neurons in the substantia nigra pars compacta and a consequent striatal dopamine deficiency. The pathogenesis of Parkinson's Disease remains unclear. Despite tremendous growth in recent years in our knowledge of the molecular basis of Parkinson's Disease and the molecular pathways of cell death important questions remain regarding why are substantia nigra cells especially vulnerable, which mechanisms underlie progressive cell loss or what do Lewy bodies or alpha-synuclein reveal about disease progression. Understanding the different vulnerability of the dopaminergic neurons from midbrain regions and the mechanisms whereby pathology becomes widespread are primary objectives of basic and clinical research in Parkinson's Disease.This e-Book discusses the etiopathogenesis of Parkinson's Disease, presenting a series of papers that provide up-to-date, state-of-the-art information on molecular and cellular mechanisms involved in the neurodegeneration process in the disease, the role of activation of functional anatomical organization of the basal ganglia and in particular habitual vs goal directed systems as a factor of neuronal vulnerability, the possibility that Parkinson's Disease coulb be a prion disease and how genetic factors linked to familial and sporadic forms of PD. We hope that this e-Book will stimulate the continuing efforts to understand the cell and physiological mechanisms underlying the origin of Parkinson's Disease.

Neuroproteomics

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ISBN: 9783039281060 9783039281077 Year: Pages: 318 DOI: 10.3390/books978-3-03928-107-7 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General) --- Neurology
Added to DOAB on : 2020-04-07 23:07:08
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The Neuroproteomics Special Issue overviews the unique challenges that must be addressed to carry out meaningful MS/proteomics analyses on neural tissues and the technologies that are available to meet these challenges. The articles on Alzheimer’s disease, addiction, and schizophrenia illustrate how MS/proteomics technologies can be used to improve our ability to diagnose and understand the molecular basis for neurological diseases. Several articles will be of interest to investigators beyond the field of neurological disorders. The review on the discovery of biofluid biomarkers of neurodegenerative dementias will be of interest to investigators searching for other disease biomarkers. Similarly, the review on the role of neuroproteomics in elucidating mechanisms of drug addiction provides an overview of the utility of MS/proteomics approaches for addressing critical questions in addiction neuroscience that should be applicable to investigators involved in virtually any area of biomedical research. Likewise, the article on developing targeted MS approaches for quantifying postsynaptic density proteins will be useful for any investigator who wishes to design targeted assays for virtually any protein. Finally, the peroxidase-mediated proximity labeling technology, described in the article on mapping the proteome of the synaptic cleft, will be of interest to investigators interested in mapping other spatially restricted proteomes.

Keywords

proteomics --- basal ganglia --- synapses --- synapse specificity --- neuronal circuits --- axons --- dendrites --- neurodegeneration --- synapse --- postsynaptic --- proteome --- mass spectrometry --- protein interaction networks --- connectome --- neurodegeneration --- Alzheimer’s disease --- cerebrospinal fluid --- plasma --- serum --- proteomics --- biomarkers --- LC-MS/MS --- cocaine --- addiction --- cytokine --- neuroimmune --- ventral tegmental area --- peptidylglycine ?-amidating monooxygenase --- cilia --- mating --- signal peptide --- prohormone convertase --- carboxypeptidase --- matrix metalloproteinase --- subtilisin --- pherophorin --- morphine --- opioid receptors --- conformational antibody --- analgesia --- GPCR signaling --- phosphorylation --- AMPA receptor complex --- transmembrane AMPA receptor regulatory protein --- synaptic plasticity --- adolescence --- corticosterone --- proteomics --- yohimbine --- progressive ratio --- reinstatement --- ethanol --- nicotinic receptor --- CaMKII --- PKA --- quantitative phosphoproteomics --- mouse --- phosphorylation --- nicotine --- proteomics --- proteome --- mass spectrometry --- Alzheimer’s disease --- protein aggregation --- laser capture microdissection --- splicing --- U1 snRNP --- synapse --- synaptic cleft --- trans-synaptic adhesion --- proximity labeling --- SynCAM --- Cadm --- Receptor-type tyrosine-protein phosphatase zeta --- R-PTP-zeta --- Ptprz1 --- neuroproteome --- drug abuse --- neuropeptidomics --- phosphorylation --- interactome --- cell type --- neuroscience --- proteomics --- mass spectrometry --- neuron --- proximity labeling --- affinity chromatography --- neuroproteomics --- biotinylation --- amphetamine --- spinophilin --- protein phosphatase-1 --- dopamine --- striatum --- mass spectroscopy --- bioinformatics --- FGF14 --- voltage gated channels --- schizophrenia --- autism --- Alzheimer’s Disease --- sex-specific differences --- synaptic plasticity --- cognitive impairment --- excitatory/inhibitory tone --- n/a --- postsynaptic density --- PSD --- parallel reaction monitoring --- PRM --- targeted proteomics --- data-independent acquisition --- DIA --- quantitative mass spectrometry --- n/a

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