12. Alterations in the Endocannabinoid System as a Link Between Unbalanced Energy Homeostasis, Neuroinflammation, and Neurological and Neuropsychiatric Disorders

  1. Tahira Farooqui and
  2. Akhlaq A. Farooqui
  1. Tiziana Bisogno and
  2. Vincenzo Di Marzo

Published Online: 11 OCT 2013

DOI: 10.1002/9781118395318.ch12

Metabolic Syndrome and Neurological Disorders

Metabolic Syndrome and Neurological Disorders

How to Cite

Bisogno, T. and Di Marzo, V. (2013) Alterations in the Endocannabinoid System as a Link Between Unbalanced Energy Homeostasis, Neuroinflammation, and Neurological and Neuropsychiatric Disorders, in Metabolic Syndrome and Neurological Disorders (eds T. Farooqui and A. A. Farooqui), John Wiley & Sons Ltd, Chichester, UK. doi: 10.1002/9781118395318.ch12

Author Information

  1. Endocannabinoid Research Group, Institute of Biomolecular Chemistry, Consiglio Nazionale delle Ricerche, Pozzuoli (NA), Italy

Publication History

  1. Published Online: 11 OCT 2013
  2. Published Print: 15 NOV 2013

ISBN Information

Print ISBN: 9781118395271

Online ISBN: 9781118395318

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Keywords:

  • Alzheimer disease;
  • chronic stress;
  • endocannabinoid system (eCB);
  • energy homeostasis;
  • metabolic disorders;
  • neuroinflammatory disorders;
  • neuropsychiatric disorders

Summary

The two most studied endocannabinoids (eCB) are anandamide and 2-arachidonoyl-glycerol (2-AG), for which metabolic routes and enzymes were identified. CB1 receptors are often expressed on presynaptic axon terminals in the brain and participate in the retrograde control of neurotransmitter release and of both short- and long-term synaptic plasticity by eCB. CB2 receptors are expressed in blood cells as well as in astrocytes and microglia, where their stimulation controls activation and cytokine release. Brain and blood alterations of this “eCB system” are observed, respectively, in experimental models of, and in patients with, obesity as well as neuroinflammatory disorders, but also during chronic stress leading to neuropsychiatric disorders. All these conditions are accompanied by disrupted activity of neurons, microglia, and astrocytes. Therefore, it is possible that a dysfunction of the eCB system in the central nervous system (CNS) may represent a link for the previously observed connections between metabolic and neuroinflammatory disorders.