Adenosine receptors and neuroinflammation

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Neuroinflammation, mainly sustained by microglial activation, is one of the hallmarks of many neurodegenerative diseases, including Parkinson’s disease, Huntington’s disease, Alzheimer’s disease, and amyotrophic lateral sclerosis. A broad spectrum of functionally distinct microglial phenotypes has been described, differently affecting the central nervous system (CNS) homeostasis. Manipulating the activation state of microglia toward neuroprotective functions can thus be of therapeutic benefit in a number of CNS diseases. Adenosine is an endogenous neuromodulator acting through the stimulation of four receptor subtypes, namely, A 1 , A 2A , A 2B , and A 3 receptors (Rs). Among its numerous effects, adenosine plays an important immunoregulatory role in the CNS. A 2A R activation, in particular, appears to play a crucial role mainly by regulating microglial function. Emerging evidence indicates that such receptors may mediate different and even opposite effects on brain inflammation according to the stage of the pathological condition and to the different inflammatory cell types involved in that particular stage. The complex role of A 2A Rs in controlling neuroinflammation is strongly dependent also on the interplay with other neurotransmitters. In this chapter, we will critically discuss the role of adenosine receptors in neuroinflammation (with particular emphasis on the A 2A R subtype), and its possible relevance to neurodegeneration.

Original languageEnglish
Pages (from-to)217-237
Number of pages21
Publication statusPublished - Jan 1 2018


  • Adenosine A receptors
  • Astrocytes
  • Central nervous system
  • Microglia
  • Neurodegenerative diseases

ASJC Scopus subject areas

  • Medicine(all)


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