Neurobiology of mental disorders

From WikiLectures

In general[edit | edit source]

  • 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

Examples of mental disorder and their neurobiological etiopathogenesis[edit | edit source]

1. Depression[edit | edit source]

  • 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[edit | edit source]

  • 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[edit | edit source]

  • 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