Neurobiology of mental disorders

In general

 * Changes in the brain signal transmission are essential in the development of mental disorders


 * genetic effects, effect of stress (environmental factors) and effect of disturbed chronobiology) - it is proposed that the bases of biological changes (plasticity, connections) are changes in neurotransmission, signal transduction and information storage and processing

1. Depression

 * Monoamine hypothesis
 * Most antidepressants work by inhibiting the reuptake of monoamines (e.g., serotonin, noradrenaline, dopamine), indicating that a lack of monoamines plays a major role in the pathophysiology of depression (and other mood disorders). MAO-A activity and density of adrenergic transporters are included in the pathophysiology → regulation of serotonin and norepinephrine levels in the brain   -
 * More recent hypothesis (low yield for examination)
 * Neurotrophic hypothesis of depression: CREB (cAMP response element binding protein) is one intracellular target of long-term antidepressant treatment and BDNF (brain-derived neurotrophic factor) is one target gene of CREB
 * Inflammatory and neurodegenerative hypothesis of depression: Depression is associated with both inflammatory processes, as well as neurodegeneration and reduced neurogenesis

2. Bipolar disease

 * hypothesis of mitochondrial dysfunction
 * calcium and mitochondrial dysfunction hypothesis
 * corresponds to the neurotrophic hypothesis → role of calcium in singaling pathway in synaptic plasticity regulation

3. Schizophrenia

 * Dopamine hypothessis
 * Dopamine excess in the mesolimbic pathway
 * Dopamine reduction in the frontocortical pathway
 * Glutamate hypothesis
 * developmental anomaly of glutamate synapse -> secondary dopaminergic dysfunction
 * NMDA antagonists mimic some positive and negative symptoms as seen in schizophrenia
 * likely both hypothesis (glumate and dopaminergic abnormalities) are implicated in that disease