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020			_a3319511521 _q(electronic bk.)
020			_a9783319511528 _q(electronic bk.)
020			_z3319511513
020			_z9783319511511
035			_a(OCoLC)967851421 _z(OCoLC)967512023 _z(OCoLC)967561388 _z(OCoLC)970389338 _z(OCoLC)974651595 _z(OCoLC)1005821755 _z(OCoLC)1011794047
040			_aIDEBK _cIDEBK _dEBLCP _dN$T _dGW5XE _dN$T _dYDX _dUAB _dOCLCF _dIOG _dWAU _dMERER _dOCLCQ _dJBG _dIAD _dICW _dICN _dILO _dAZU _dCOO _dDKU _dUPM _dOCLCO _dOCLCQ _dVT2 _dOCLCO _dJG0 _dOCLCO _dOCLCA _dU3W _dES-MaUEC _bspa
050		4	_aRC537 _b.I545 2017 EB
245	0	0	_aInflammation-associated depression : _bevidence, mechanisms and implications _cRobert Dantzer, Lucile Capuron, editors.
264		1	_a[Lugar de publicación no identificado] _bSpringer _c2017
300			_a1 recurso en línea (x, 356 páginas) _bilustraciones
336			_aTexto _btxt _2rdacontent
337			_aelectrónico _bc _2rdamedia
338			_arecurso electrónico _bcr _2rdacarrier
347			_atext file _bPDF _2rda
490	0		_aCurrent topics in behavioral neurosciences _x1866-3370 _vvolume 31
500			_aSpringerLink _bSpringer Biomedical and Life Sciences eBooks 2017 English+International
505	0		_aPreface; Contents; Evidence for Inflammation-Associated Depression; 1 Introduction; 2 Evidence from Animal Models; 3 Evidence from Clinical Studies; 3.1 Cytokines and Cell-Mediated Immune (CMI) Pathways Contribute to Inflammation and Depression; 3.2 Platelet-Activating Factors (PAFs) and Oxidative and Nitrosative Stress (OandNS) Contribute to Inflammation and Depression; 3.3 Damage to Mitochondria and Mitochondrial DNA Contribute to Inflammation and Depression; 4 Discussion; 5 Conclusion; References.
505	8		_a1.4 Peripheral Immune-Cell-to-Brain Signaling2 Changes in Brain Function as a Result of Periphery-to-Brain Communication; 3 Gut Microbiome, Systemic Inflammation, and Altered Behavior and Mood; 3.1 Gut Microbiome and Changes During Inflammatory Diseases; 3.2 Gut-to-Brain Communication Can Modulate Behavior; 3.3 Changes in Gut Microbiome Can Modulate Systemic Inflammation and Thereby Behavior; 3.4 Gut Dysbiosis in Systemic Disease; 4 Concluding Remarks; References; Mechanisms of Inflammation-Associated Depression: Immune Influences on Tryptophan and Phenylalanine Metabolisms; 1 Introduction.
505	8		_a4.2 Inflammation and Cardiovascular Disease4.3 C-Reactive Protein; 4.4 Endothelial Dysfunction; 5 The Tryptophan/Kynurenine Pathway: Implications for Serotonergic Transmission; 6 Inflammation and the Serotonin Transporter; 7 The Glutamatergic Theory of Depression; 8 Other Mechanisms; 9 Treatment Issues; 10 Concluding Remarks; References; Immune-to-Brain Communication Pathways in Inflammation-Associated Sickness and Depression; 1 Periphery-to-Brain Communication Pathways; 1.1 Neural Pathway; 1.2 Signaling via Cerebral Endothelial Cells; 1.3 Signaling via the Circumventricular Organs.
505	8		_aPersonality3 Conclusion and Therapeutic Implications; References; Inflammation-Associated Co-morbidity Between Depression and Cardiovascular Disease; 1 Introduction; 2 Epidemiology; 2.1 Depressive Illness; 2.2 Cardiovascular Disease; 2.3 Co-morbidity Between DI and Cardiovascular Disease; 3 Factors Accountable for the Co-morbidity; 3.1 Role of Stress in Inflammation and Depression; 3.2 Autonomic Nervous System Dysfunction; 3.3 Heart Rate Variability; 4 Bidirectionality of Inflammation in Cardiovascular Disease and Depression; 4.1 Inflammation and Depression.
505	8		_aRole of Inflammation in the Development of Neuropsychiatric Symptom Domains: Evidence and Mechanisms1 Inflammation and Neuropsychiatric Symptoms; 1.1 From Sickness to Neuropsychiatric Disorders; 1.2 Towards the Identification of Common Major Symptom Domains Targeted by Inflammatory Processes; 1.3 Evidence for a Role of Inflammation in Distinct Neuropsychiatric Domains; 2 Inflammation and the Specificity of Neuropsychiatric Symptoms Units; 2.1 A Multimodal Biological Substrate; 2.2 Vulnerability and Modulatory Factors; The HPA Axis and Its Relation to Stress; Metabolic Abnormalities.
520	3		_aInflammation has invaded the field of psychiatry. The finding that cytokines are elevated in various affective and psychotic disorders brings to the forefront the necessity of identifying the precise research domain criteria (RDoCs) that inflammation is responsible for. This task is certainly the most advanced in major depressive disorders. The reason is that a dearth of clinical and preclinical studies has demonstrated that inflammation can cause symptoms of depression and conversely, cytokine antagonists can attenuate symptoms of depression in medical and psychiatric patients with chronic low grade inflammation. Important knowledge has been gained on the symptom dimensions that inflammation is driving and the mechanisms of action of cytokines in the brain, providing new targets for drug research and development. The aim of the book ℓ́ℓInflammation-Associated Depressionℓ́ℓ is to present this field of research and its implications in a didactic and comprehensive manner to basic and clinical scientists, psychiatrists, physicians, and students at the graduate level.
650		7	_aDepresión mental _2embne _0(OCoLC)fst00890931 _0 _9138611
700	1		_aCapuron, Lucile.
700	1		_aDantzer, Robert. _95536
856	4	0	_uhttps://go.openathens.net/redirector/universidadeuropea.es?url=http://link.springer.com/10.1007/978-3-319-51152-8 _zAcceso a este recurso digital (usuarios Universidad Europea de Madrid)
988			_aEBOOK, asignarmaterias, EBSPRINGER_2017B
998			_b02/2018 _dz _e- _zSI
999			_c95164 _d95164 _x1