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Novel neuroprotection by caffeine and adenosine A(2A) receptor antagonists in animal models of Parkinson's disease.
J Neurol Sci. 2006 Oct 25; 248(1-2):9-15.JN

Abstract

The adenosine A(2A) receptor has recently emerged as a leading non-dopaminergic therapeutic target for Parkinson's disease, largely due to the restricted distribution of the receptor in the striatum and the profound interaction between adenosine and dopamine receptors in brain. Two lines of research in particular have demonstrated the promise of the A(2A) receptor antagonists as novel anti-parkinsonian drugs. First, building on extensive preclinical animal studies, the A(2A) receptor antagonist KW6002 has demonstrated its potential to increase motor activity in PD patients of the advanced stage in a recent clinical phase IIB trial. Second, recently two prospective epidemiological studies of large cohorts have firmly established the inverse relationship between the consumption of caffeine (a non-specific adenosine antagonist) and the risk of developing PD. The potential neuroprotective effect of caffeine and A(2A) receptor antagonists in PD is further substantiated by the demonstration that pharmacological blockade (by caffeine or specific A(2A) antagonists) or genetic depletion of the A(2A) receptor attenuated dopaminergic neurotoxicity and neurodegeneration in animal models of PD. Moreover, A(2A) receptor antagonism-mediated neuroprotection goes beyond PD models and can be extended to a variety of other brain injuries induced by stroke, excitotoxicity and mitochondrial toxins. Intensive investigations are under way to dissect out common cellular mechanisms (such as A(2A) receptor modulation of neuroinflammation) which may underlie the broad spectrum of neuroprotection by A(2A) receptor inactivation in brain.

Authors+Show Affiliations

Molecular Neuropharmacology Lab, Department of Neurology, Boston University Medical Center, Boston, MA 02118, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Review

Language

eng

PubMed ID

16806272

Citation

Kalda, Anti, et al. "Novel Neuroprotection By Caffeine and Adenosine A(2A) Receptor Antagonists in Animal Models of Parkinson's Disease." Journal of the Neurological Sciences, vol. 248, no. 1-2, 2006, pp. 9-15.
Kalda A, Yu L, Oztas E, et al. Novel neuroprotection by caffeine and adenosine A(2A) receptor antagonists in animal models of Parkinson's disease. J Neurol Sci. 2006;248(1-2):9-15.
Kalda, A., Yu, L., Oztas, E., & Chen, J. F. (2006). Novel neuroprotection by caffeine and adenosine A(2A) receptor antagonists in animal models of Parkinson's disease. Journal of the Neurological Sciences, 248(1-2), 9-15.
Kalda A, et al. Novel Neuroprotection By Caffeine and Adenosine A(2A) Receptor Antagonists in Animal Models of Parkinson's Disease. J Neurol Sci. 2006 Oct 25;248(1-2):9-15. PubMed PMID: 16806272.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Novel neuroprotection by caffeine and adenosine A(2A) receptor antagonists in animal models of Parkinson's disease. AU - Kalda,Anti, AU - Yu,Liqun, AU - Oztas,Emin, AU - Chen,Jiang-Fan, Y1 - 2006/06/27/ PY - 2006/6/30/pubmed PY - 2007/1/24/medline PY - 2006/6/30/entrez SP - 9 EP - 15 JF - Journal of the neurological sciences JO - J Neurol Sci VL - 248 IS - 1-2 N2 - The adenosine A(2A) receptor has recently emerged as a leading non-dopaminergic therapeutic target for Parkinson's disease, largely due to the restricted distribution of the receptor in the striatum and the profound interaction between adenosine and dopamine receptors in brain. Two lines of research in particular have demonstrated the promise of the A(2A) receptor antagonists as novel anti-parkinsonian drugs. First, building on extensive preclinical animal studies, the A(2A) receptor antagonist KW6002 has demonstrated its potential to increase motor activity in PD patients of the advanced stage in a recent clinical phase IIB trial. Second, recently two prospective epidemiological studies of large cohorts have firmly established the inverse relationship between the consumption of caffeine (a non-specific adenosine antagonist) and the risk of developing PD. The potential neuroprotective effect of caffeine and A(2A) receptor antagonists in PD is further substantiated by the demonstration that pharmacological blockade (by caffeine or specific A(2A) antagonists) or genetic depletion of the A(2A) receptor attenuated dopaminergic neurotoxicity and neurodegeneration in animal models of PD. Moreover, A(2A) receptor antagonism-mediated neuroprotection goes beyond PD models and can be extended to a variety of other brain injuries induced by stroke, excitotoxicity and mitochondrial toxins. Intensive investigations are under way to dissect out common cellular mechanisms (such as A(2A) receptor modulation of neuroinflammation) which may underlie the broad spectrum of neuroprotection by A(2A) receptor inactivation in brain. SN - 0022-510X UR - https://www.unboundmedicine.com/medline/citation/16806272/Novel_neuroprotection_by_caffeine_and_adenosine_A_2A__receptor_antagonists_in_animal_models_of_Parkinson's_disease_ DB - PRIME DP - Unbound Medicine ER -