Neuronal insulin Receptor Signaling a Potential Target For The Treatment of Cognitive and Mood Disorders

Mood disorders are a crucial group of mental disorders that last for a life time, cause psychosocial dysfunction, disrupts interpersonal relationships and are overall highly restrictive. The facts that mood disorders are seen as high as 3-5% of the society and 70% of the patients' first psychiatric application puts forward that they are not well known show that these are a serious type of mental illness. The average time to make the right diagnose is reported as 10 years. The delays in diagnose and beginning of treatment lays a heavy burden on the patient, their relatives and society in general. After the diagnose begins the process of selecting the right treatment method of each individual which is of high importance as to enable the patient go through their treatment period without mental exhaustion. Protecting treatment planning and management in long term treatments are significant for the control of the disorder. Difficulties are frequently experience during diagnose, treatment and follow up for mood disorders. Professional constantly seek for innovations to resolve these issues in treating mood disorders. In this context, we hope that this book will become an important resource of some new researches for clinicians. Cover......Page 1 Mood Disorders......Page 2 ©......Page 3 Contents......Page 5 Preface......Page 7 1. Introduction......Page 9 3. Matherials and methods......Page 14 4. Results and discussion......Page 15 6. Conclusions......Page 27 References......Page 28 2.1. The epidemiology of depression and diabetes......Page 31 2.2. Clinical symptoms......Page 33 2.3.1. Risk factors for depression in patients with diabetes......Page 34 2.3.2. Depression - a risk factor for diabetes?......Page 36 3. The common pathophysiological mechanisms of depression and diabetes......Page 37 3.2. Depression with diabetes: the result of psychosocial factors in relation to DM......Page 39 3.3. Depression with diabetes: a risk factor for the origin and worsening course of the result of DM......Page 40 4. The treatment of comorbidity depression and diabetes......Page 41 4.1. Pharmacological studies......Page 43 5. Discussion......Page 46 6. Conclusion......Page 47 References......Page 48 1.1. Introduction: Surface symptoms and aetiology......Page 55 2. The effects of the diagnostic and statistical manual on the homogenisation and simplification of mental illness and in particular depression......Page 58 3. An “Epidemic” of depression?......Page 61 4. The phenomenology of depression across cultures and the westernisation of mental illness: The case of Japan......Page 62 5. Westernisation of depression the role of “big pharma”......Page 63 6. A way forward......Page 64 References......Page 65 1. Introduction......Page 69 2. Symptoms of depression......Page 71 3. Epidemiology and co-morbidity of depressive disorders......Page 72 4. Classification and diagnostics of depressive disorder......Page 73 5. Brief history of CBT......Page 74 6.2. SORCK model of behavioral analysis......Page 76 7. Psychological generation models of depressive disorders......Page 77 7.1.1. Cognition-theoretical explanation model according to Beck......Page 78 7.2. Learning and behavior-theoretical models......Page 79 7.3. Integrative models......Page 80 8.1. Building-up daily activities......Page 81 8.2. Social competence training......Page 86 8.2.1. Performance of social competence training......Page 87 8.2.2. Problem-solving training......Page 90 8.2.3. Helping behavior......Page 91 8.3. Cognitive techniques......Page 92 8.3.1.2. Socratic dialogue......Page 93 8.3.2. Change NATs......Page 95 8.4. Completion of therapy, relapse prophylaxis......Page 98 References......Page 99 1. Introduction......Page 109 2. Mitochondria......Page 110 2.1. Physiology of oxidative phosphorylation......Page 111 2.1.1. Oxidative phosphorylation enzymes......Page 113 2.1.2. Monoamine oxidase......Page 114 2.2. Regulation of OXPHOS......Page 115 2.3.1. Fatty acids......Page 118 2.4. Reactive oxygen species production......Page 119 2.6. Specific inhibitors of complexes of ETC......Page 120 2.7. Mitochondria and neuroplasticity......Page 121 3.1. Monoamine hypothesis......Page 123 3.2. Neurotrophic hypothesis......Page 124 3.5. Biological markers of mood disorders......Page 125 4. Antidepressants, mood stabilizers and mitochondrial functions......Page 126 4.1. Inhibition of MAO......Page 127 4.2. Effects of antidepressants on mitochondrial functions......Page 128 4.3. Effects of mood stabilizers on mitochondrial functions......Page 129 Acknowledgment......Page 133 References......Page 134 1. Introduction......Page 153 2.1. Chronic effects of the first generation of ADs on the 5-HT system......Page 155 2.2. Chronic effects of the SSRIs on the 5-HT system......Page 158 2.3. Chronic effects of new antidepressant strategies......Page 159 3.1. Neurogenesis......Page 161 3.2. Synaptic plasticity and synaptogenesis......Page 163 References......Page 165 References......Page 166 4. Conclusion......Page 167 Author details......Page 168 References......Page 169 1. Introduction......Page 189 2.1.1. Serotonergic system......Page 190 2.1.2. Noradrenergic and dopaminergic systems......Page 191 2.3. Neuroplasticity......Page 192 2.4. Neuroimaging marker......Page 194 Author details......Page 195 References......Page 196 1. Introduction......Page 205 2.1. Postnatal period and postnatal depression......Page 206 2.1.1. Impact of maternal depression on infant......Page 207 2.1.2. Impact of maternal depression on mother – infant interaction......Page 209 2.2. Midwifery skills that enhance mother-infant relationship......Page 211 2.2.1. Touch and infant massage......Page 212 2.2.2. Mother-infant relationship and newborn behavioural observation......Page 213 2.3.1. Methodology......Page 214 3. Discussion and conclusions......Page 215 References......Page 216 2.1. Subjects......Page 229 2.2.1. Cognitive tests: Paper-and-pencil tests......Page 230 2.2.2. Cognitive tests: Selected tests from the Cambridge automated neuropsychological test battery......Page 231 3. Results......Page 232 3.1. Assessment of attention, working memory and executive functions......Page 233 4.1. Cognitive functions in bipolar patients......Page 235 4.2. Factors associated with cognitive deficits......Page 237 Author details......Page 240 References......Page 241 1. Introduction......Page 249 2. Fatty acids in the brain and nervous system......Page 250 3. DHA in the brain cells......Page 251 3.2. The role of DHA in membrane neuronal function......Page 252 3.4. Inhibition of neuronal apoptosis by DHA......Page 253 3.5. DHA and the regulation of gene expression in neurons......Page 254 4.1. Alzheimer’s disease......Page 255 4.2. Depression and postpartum depression......Page 256 4.4. Aggression, hostility and anti-social behavior......Page 258 5. Possible mechanism for links between DHA and mood disorders......Page 259 6.1. Free DHA and DHA-ethyl ester......Page 260 6.4. sn-2 DHA monoacylglyceride......Page 261 7. Conclusions and future prospects......Page 262 References......Page 263 1. Introduction......Page 271 2. Insulin and insulin receptor signaling in the brain......Page 272 3. Physiological roles of insulin in the brain......Page 273 4. Insulin resistance and cognitive disorders......Page 274 5. Insulin resistance and mood disorders......Page 275 6. Intranasal administration of insulin......Page 276 7.1. Nicotine and protein kinase C-α (PKC-α) activation: enhancement of insulin receptor signaling via increase in IRS-1, IRS-2, and cell surface insulin receptor (Fig.1 1 and 1').......Page 277 7.2. Immunosuppressants, cyclosporine and tacrolimus: reduction of insulin receptor signaling via down-regulation of cell surface insulin receptor and IRS-2. (Fig.12)......Page 279 7.3. Ketone body acetoacetate: reduction of insulin receptor signaling via down-regulation of cell surface insulin receptor. (Fig.13)......Page 280 7.4. Hsp90 inhibitors: impairment of insulin receptor signaling via down-regulation of cell surface insulin receptor and various downstream signaling molecules. (Fig.14)......Page 281 7.5. Insulin, IGF-1 and potent GSK-3 inhibitors (lithium and valproic acid): negative feedback regulation of insulin receptor signaling. (Fig.1 5 and 5’)......Page 283 8. Conclusion and future perspectives......Page 284 References......Page 285