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Br J Pharmacol. 2003 Apr;138(7):1207-9.

Neuroprotection by caffeine and adenosine A2A receptor blockade of beta-amyloid neurotoxicity.

Author information

1
Department of Biochemistry, Federal University of Rio Grande do Sul, Porto Alegre, Brazil.

Erratum in

  • Br J Pharmacol. 2003 Jul;139(8):1571. Dall'lgna Oscar P [corrected to Dall'Igna].

Abstract

Adenosine is a neuromodulator in the nervous system and it has recently been observed that pharmacological blockade or gene disruption of adenosine A(2A) receptors confers neuroprotection under different neurotoxic situations in the brain. We now observed that coapplication of either caffeine (1-25 micro M) or the selective A(2A) receptor antagonist, 4-(2-[7-amino-2(2-furyl)(1,2,4)triazolo (2,3-a)(1,3,5)triazin-5-ylamino]ethyl)phenol (ZM 241385, 50 nM), but not the A receptor antagonist, 8-cyclopentyltheophylline (200 nM), prevented the neuronal cell death caused by exposure of rat cultured cerebellar granule neurons to fragment 25-35 of beta-amyloid protein (25 micro M for 48 h), that by itself caused a near three-fold increase of propidium iodide-labeled cells. This constitutes the first in vitro evidence to suggest that adenosine A(2A) receptors may be the molecular target responsible for the observed beneficial effects of caffeine consumption in the development of Alzheimer's disease.

PMID:
12711619
PMCID:
PMC1573785
DOI:
10.1038/sj.bjp.0705185
[Indexed for MEDLINE]
Free PMC Article

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