Neuroprotection by caffeine and A(2A) adenosine receptor inactivation in a model of Parkinson's disease
Recent epidemiological studies have established an association between the common consumption of coffee or other caffeinated beverages and a reduced risk of developing Parkinson's disease (PD). To explore the possibility that caffeine helps prevent the dopaminergic deficits characteristic of PD...
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| Veröffentlicht in: | The Journal of neuroscience 2001-05, Vol.21 (10), p.RC143 |
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| creator | Chen, J F Xu, K Petzer, J P Staal, R Xu, Y H Beilstein, M Sonsalla, P K Castagnoli, K Castagnoli, Jr, N Schwarzschild, M A |
| description | Recent epidemiological studies have established an association between the common consumption of coffee or other caffeinated beverages and a reduced risk of developing Parkinson's disease (PD). To explore the possibility that caffeine helps prevent the dopaminergic deficits characteristic of PD, we investigated the effects of caffeine and the adenosine receptor subtypes through which it may act in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxin model of PD. Caffeine, at doses comparable to those of typical human exposure, attenuated MPTP-induced loss of striatal dopamine and dopamine transporter binding sites. The effects of caffeine were mimicked by several A(2A) antagonists (7-(2-phenylethyl)-5-amino-2-(2-furyl)-pyrazolo-[4,3-e]-1,2,4-triazolo[1,5-c]pyrimidine (SCH 58261), 3,7-dimethyl-1-propargylxanthine, and (E)-1,3-diethyl-8 (KW-6002)-(3,4-dimethoxystyryl)-7-methyl-3,7-dihydro-1H-purine-2,6-dione) (KW-6002) and by genetic inactivation of the A(2A) receptor, but not by A(1) receptor blockade with 8-cyclopentyl-1,3-dipropylxanthine, suggesting that caffeine attenuates MPTP toxicity by A(2A) receptor blockade. These data establish a potential neural basis for the inverse association of caffeine with the development of PD, and they enhance the potential of A(2A) antagonists as a novel treatment for this neurodegenerative disease. |
| doi_str_mv | 10.1523/jneurosci.21-10-j0001.2001 |
| format | Article |
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To explore the possibility that caffeine helps prevent the dopaminergic deficits characteristic of PD, we investigated the effects of caffeine and the adenosine receptor subtypes through which it may act in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxin model of PD. Caffeine, at doses comparable to those of typical human exposure, attenuated MPTP-induced loss of striatal dopamine and dopamine transporter binding sites. The effects of caffeine were mimicked by several A(2A) antagonists (7-(2-phenylethyl)-5-amino-2-(2-furyl)-pyrazolo-[4,3-e]-1,2,4-triazolo[1,5-c]pyrimidine (SCH 58261), 3,7-dimethyl-1-propargylxanthine, and (E)-1,3-diethyl-8 (KW-6002)-(3,4-dimethoxystyryl)-7-methyl-3,7-dihydro-1H-purine-2,6-dione) (KW-6002) and by genetic inactivation of the A(2A) receptor, but not by A(1) receptor blockade with 8-cyclopentyl-1,3-dipropylxanthine, suggesting that caffeine attenuates MPTP toxicity by A(2A) receptor blockade. These data establish a potential neural basis for the inverse association of caffeine with the development of PD, and they enhance the potential of A(2A) antagonists as a novel treatment for this neurodegenerative disease.</description><identifier>EISSN: 1529-2401</identifier><identifier>DOI: 10.1523/jneurosci.21-10-j0001.2001</identifier><identifier>PMID: 11319241</identifier><language>eng</language><publisher>United States</publisher><subject><![CDATA[1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine - antagonists & inhibitors ; 3,4-Dihydroxyphenylacetic Acid - metabolism ; Animals ; Caffeine - administration & dosage ; Catechols - metabolism ; Corpus Striatum - drug effects ; Corpus Striatum - metabolism ; Corpus Striatum - pathology ; Disease Models, Animal ; Dopamine - metabolism ; Dose-Response Relationship, Drug ; Immunity, Innate - genetics ; Injections, Intraperitoneal ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neuroprotective Agents - administration & dosage ; Parkinsonian Disorders - chemically induced ; Parkinsonian Disorders - drug therapy ; Parkinsonian Disorders - genetics ; Purinergic P1 Receptor Antagonists ; Purines - administration & dosage ; Pyrimidines - administration & dosage ; Receptor, Adenosine A2A ; Receptors, Purinergic P1 - deficiency ; Receptors, Purinergic P1 - genetics ; Theobromine - administration & dosage ; Theobromine - analogs & derivatives ; Triazoles - administration & dosage ; Xanthines - administration & dosage]]></subject><ispartof>The Journal of neuroscience, 2001-05, Vol.21 (10), p.RC143</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c321t-d34fc15655c6845250fc6bdc00bd42cd0ce40f09a6ea555ebfdbe59a77176c513</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11319241$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, J F</creatorcontrib><creatorcontrib>Xu, K</creatorcontrib><creatorcontrib>Petzer, J P</creatorcontrib><creatorcontrib>Staal, R</creatorcontrib><creatorcontrib>Xu, Y H</creatorcontrib><creatorcontrib>Beilstein, M</creatorcontrib><creatorcontrib>Sonsalla, P K</creatorcontrib><creatorcontrib>Castagnoli, K</creatorcontrib><creatorcontrib>Castagnoli, Jr, N</creatorcontrib><creatorcontrib>Schwarzschild, M A</creatorcontrib><title>Neuroprotection by caffeine and A(2A) adenosine receptor inactivation in a model of Parkinson's disease</title><title>The Journal of neuroscience</title><addtitle>J Neurosci</addtitle><description>Recent epidemiological studies have established an association between the common consumption of coffee or other caffeinated beverages and a reduced risk of developing Parkinson's disease (PD). To explore the possibility that caffeine helps prevent the dopaminergic deficits characteristic of PD, we investigated the effects of caffeine and the adenosine receptor subtypes through which it may act in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxin model of PD. Caffeine, at doses comparable to those of typical human exposure, attenuated MPTP-induced loss of striatal dopamine and dopamine transporter binding sites. The effects of caffeine were mimicked by several A(2A) antagonists (7-(2-phenylethyl)-5-amino-2-(2-furyl)-pyrazolo-[4,3-e]-1,2,4-triazolo[1,5-c]pyrimidine (SCH 58261), 3,7-dimethyl-1-propargylxanthine, and (E)-1,3-diethyl-8 (KW-6002)-(3,4-dimethoxystyryl)-7-methyl-3,7-dihydro-1H-purine-2,6-dione) (KW-6002) and by genetic inactivation of the A(2A) receptor, but not by A(1) receptor blockade with 8-cyclopentyl-1,3-dipropylxanthine, suggesting that caffeine attenuates MPTP toxicity by A(2A) receptor blockade. These data establish a potential neural basis for the inverse association of caffeine with the development of PD, and they enhance the potential of A(2A) antagonists as a novel treatment for this neurodegenerative disease.</description><subject>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine - antagonists & inhibitors</subject><subject>3,4-Dihydroxyphenylacetic Acid - metabolism</subject><subject>Animals</subject><subject>Caffeine - administration & dosage</subject><subject>Catechols - metabolism</subject><subject>Corpus Striatum - drug effects</subject><subject>Corpus Striatum - metabolism</subject><subject>Corpus Striatum - pathology</subject><subject>Disease Models, Animal</subject><subject>Dopamine - metabolism</subject><subject>Dose-Response Relationship, Drug</subject><subject>Immunity, Innate - genetics</subject><subject>Injections, Intraperitoneal</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Neuroprotective Agents - administration & dosage</subject><subject>Parkinsonian Disorders - chemically induced</subject><subject>Parkinsonian Disorders - drug therapy</subject><subject>Parkinsonian Disorders - genetics</subject><subject>Purinergic P1 Receptor Antagonists</subject><subject>Purines - administration & dosage</subject><subject>Pyrimidines - administration & dosage</subject><subject>Receptor, Adenosine A2A</subject><subject>Receptors, Purinergic P1 - deficiency</subject><subject>Receptors, Purinergic P1 - genetics</subject><subject>Theobromine - administration & dosage</subject><subject>Theobromine - analogs & derivatives</subject><subject>Triazoles - administration & dosage</subject><subject>Xanthines - administration & dosage</subject><issn>1529-2401</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1j81LAzEQxYMgtlb_BQle1MPWmexm1z0W8QuKetBzmU0mktomS7IV-t_b-nF5D-a938AT4hxhilqV18vAmxSz8VOFBUKxBACcqp0ciPGu0RaqAhyJ45z3UQPYHIkRYomtqnAsPp73fJ_iwGbwMchuKw05xz6wpGDl7FLNriRZDjHvb4kN90NM0gfaEV_0Q_kgSa6j5ZWMTr5S-vQhx3CRpfWZKfOJOHS0ynz65xPxfn_3dvtYzF8enm5n88KUCofClpUzqGutTX1TaaXBmbqzBqCzlTIWDFfgoKWaSWvNnbMd65aaBpvaaCwn4uz3b7_p1mwXffJrStvF_-LyG8goWyQ</recordid><startdate>20010515</startdate><enddate>20010515</enddate><creator>Chen, J F</creator><creator>Xu, K</creator><creator>Petzer, J P</creator><creator>Staal, R</creator><creator>Xu, Y H</creator><creator>Beilstein, M</creator><creator>Sonsalla, P K</creator><creator>Castagnoli, K</creator><creator>Castagnoli, Jr, N</creator><creator>Schwarzschild, M A</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>20010515</creationdate><title>Neuroprotection by caffeine and A(2A) adenosine receptor inactivation in a model of Parkinson's disease</title><author>Chen, J F ; Xu, K ; Petzer, J P ; Staal, R ; Xu, Y H ; Beilstein, M ; Sonsalla, P K ; Castagnoli, K ; Castagnoli, Jr, N ; Schwarzschild, M A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c321t-d34fc15655c6845250fc6bdc00bd42cd0ce40f09a6ea555ebfdbe59a77176c513</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine - antagonists & inhibitors</topic><topic>3,4-Dihydroxyphenylacetic Acid - metabolism</topic><topic>Animals</topic><topic>Caffeine - administration & dosage</topic><topic>Catechols - metabolism</topic><topic>Corpus Striatum - drug effects</topic><topic>Corpus Striatum - metabolism</topic><topic>Corpus Striatum - pathology</topic><topic>Disease Models, Animal</topic><topic>Dopamine - metabolism</topic><topic>Dose-Response Relationship, Drug</topic><topic>Immunity, Innate - genetics</topic><topic>Injections, Intraperitoneal</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Neuroprotective Agents - administration & dosage</topic><topic>Parkinsonian Disorders - chemically induced</topic><topic>Parkinsonian Disorders - drug therapy</topic><topic>Parkinsonian Disorders - genetics</topic><topic>Purinergic P1 Receptor Antagonists</topic><topic>Purines - administration & dosage</topic><topic>Pyrimidines - administration & dosage</topic><topic>Receptor, Adenosine A2A</topic><topic>Receptors, Purinergic P1 - deficiency</topic><topic>Receptors, Purinergic P1 - genetics</topic><topic>Theobromine - administration & dosage</topic><topic>Theobromine - analogs & derivatives</topic><topic>Triazoles - administration & dosage</topic><topic>Xanthines - administration & dosage</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, J F</creatorcontrib><creatorcontrib>Xu, K</creatorcontrib><creatorcontrib>Petzer, J P</creatorcontrib><creatorcontrib>Staal, R</creatorcontrib><creatorcontrib>Xu, Y H</creatorcontrib><creatorcontrib>Beilstein, M</creatorcontrib><creatorcontrib>Sonsalla, P K</creatorcontrib><creatorcontrib>Castagnoli, K</creatorcontrib><creatorcontrib>Castagnoli, Jr, N</creatorcontrib><creatorcontrib>Schwarzschild, M A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>The Journal of neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, J F</au><au>Xu, K</au><au>Petzer, J P</au><au>Staal, R</au><au>Xu, Y H</au><au>Beilstein, M</au><au>Sonsalla, P K</au><au>Castagnoli, K</au><au>Castagnoli, Jr, N</au><au>Schwarzschild, M A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuroprotection by caffeine and A(2A) adenosine receptor inactivation in a model of Parkinson's disease</atitle><jtitle>The Journal of neuroscience</jtitle><addtitle>J Neurosci</addtitle><date>2001-05-15</date><risdate>2001</risdate><volume>21</volume><issue>10</issue><spage>RC143</spage><pages>RC143-</pages><eissn>1529-2401</eissn><abstract>Recent epidemiological studies have established an association between the common consumption of coffee or other caffeinated beverages and a reduced risk of developing Parkinson's disease (PD). To explore the possibility that caffeine helps prevent the dopaminergic deficits characteristic of PD, we investigated the effects of caffeine and the adenosine receptor subtypes through which it may act in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxin model of PD. Caffeine, at doses comparable to those of typical human exposure, attenuated MPTP-induced loss of striatal dopamine and dopamine transporter binding sites. The effects of caffeine were mimicked by several A(2A) antagonists (7-(2-phenylethyl)-5-amino-2-(2-furyl)-pyrazolo-[4,3-e]-1,2,4-triazolo[1,5-c]pyrimidine (SCH 58261), 3,7-dimethyl-1-propargylxanthine, and (E)-1,3-diethyl-8 (KW-6002)-(3,4-dimethoxystyryl)-7-methyl-3,7-dihydro-1H-purine-2,6-dione) (KW-6002) and by genetic inactivation of the A(2A) receptor, but not by A(1) receptor blockade with 8-cyclopentyl-1,3-dipropylxanthine, suggesting that caffeine attenuates MPTP toxicity by A(2A) receptor blockade. These data establish a potential neural basis for the inverse association of caffeine with the development of PD, and they enhance the potential of A(2A) antagonists as a novel treatment for this neurodegenerative disease.</abstract><cop>United States</cop><pmid>11319241</pmid><doi>10.1523/jneurosci.21-10-j0001.2001</doi><oa>free_for_read</oa></addata></record> |
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| subjects | 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine - antagonists & inhibitors 3,4-Dihydroxyphenylacetic Acid - metabolism Animals Caffeine - administration & dosage Catechols - metabolism Corpus Striatum - drug effects Corpus Striatum - metabolism Corpus Striatum - pathology Disease Models, Animal Dopamine - metabolism Dose-Response Relationship, Drug Immunity, Innate - genetics Injections, Intraperitoneal Male Mice Mice, Inbred C57BL Mice, Knockout Neuroprotective Agents - administration & dosage Parkinsonian Disorders - chemically induced Parkinsonian Disorders - drug therapy Parkinsonian Disorders - genetics Purinergic P1 Receptor Antagonists Purines - administration & dosage Pyrimidines - administration & dosage Receptor, Adenosine A2A Receptors, Purinergic P1 - deficiency Receptors, Purinergic P1 - genetics Theobromine - administration & dosage Theobromine - analogs & derivatives Triazoles - administration & dosage Xanthines - administration & dosage |
| title | Neuroprotection by caffeine and A(2A) adenosine receptor inactivation in a model of Parkinson's disease |
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