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Contribution of microglia‐mediated neuroinflammation to retinal degenerative diseases
Author(s) -
Boia R.,
Madeira M.H.,
Aires I.D.,
Neves C.R.,
Ambrósio A.F.,
Santiago A.R.
Publication year - 2017
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2017.03622
Subject(s) - neuroinflammation , microglia , adenosine a2a receptor , neuroscience , neuroprotection , retina , retinal ganglion cell , medicine , retinal , pharmacology , inflammation , adenosine receptor , receptor , immunology , biology , ophthalmology , agonist
Summary Glaucoma is characterized by optic nerve damage and retinal ganglion cell ( RGC ) loss. The onset of the disease is accompanied by microglia reactivity and neuroinflammation. Hence, therapeutic strategies designed at reducing microglia reactivity may offer therapeutic benefits to manage glaucomatous damage. We have been evaluating the ability of adenosine A 2A receptors (A 2 A R ) blockade in the control of retinal neuroinflammation and neuroprotection in experimental models of glaucoma. The pharmacological blockade or the genetic inactivation (si RNA in microglial cells or A 2 A R knockout animal) prevent microglia reactivity, retinal neuroinflammation, and RGC loss. Also, the treatment with a selective A 2 A R antagonist reverts inflammation and protects the retina. Furthermore, the intake of caffeine, a non‐selective antagonist of adenosine receptors, affords protection to the retina and prevents microglia reactivity. Our results open the possibility for the use of A 2 A R antagonists as therapeutic options in glaucoma. Funding FCT ( PTDC / BIM ‐ MEC /0913/2012, PE st‐C/ SAU / UI 3282/2011‐2013, UID / NEU /04539/2013), COMPETE ‐ FEDER ( FCOMP ‐01‐0124‐ FEDER ‐028417), Centro 2020 Regional Operational Programme ( CENTRO ‐01‐0145‐ FEDER ‐8: BrainHealth 2020) , AIBILI