We examined effects of depressive disorder and/or Alzheimer's disease (AD) on both mitochondrial enzyme activities (citrate synthase, complexes of electron transport chain) and cellular respiration in blood platelets. Results suggest that insufficient substrate availability, rather than ETS functional disturbances, is responsible for decreased mitochondrial respiration.
It can be concluded that changes of mitochondrial functions participate in the pathophysiology of depression and AD. Their modulation can contribute to therapeutic and/or adverse effects of antidepressants and mood stabilizers.