Calcium Channel Antagonists as Disease-Modifying Therapy for Parkinson’s Disease: Therapeutic Rationale and Current Status
Parkinson’s disease is a disabling hypokinetic neurological movement disorder in which the aetiology is unknown in the majority of cases. Current pharmacological treatments, though effective at restoring movement, are only symptomatic and do nothing to slow disease progression. Electrophysiological,...
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| Veröffentlicht in: | CNS drugs 2016-12, Vol.30 (12), p.1127-1135 |
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| creator | Swart, Tara Hurley, Michael J. |
| description | Parkinson’s disease is a disabling hypokinetic neurological movement disorder in which the aetiology is unknown in the majority of cases. Current pharmacological treatments, though effective at restoring movement, are only symptomatic and do nothing to slow disease progression. Electrophysiological, epidemiological and neuropathological studies have implicated Ca
V
1.3 subtype calcium channels in the pathogenesis of the disorder, and drugs with some selectivity for this ion channel (brain-penetrant dihydropyridine calcium channel blockers) are neuroprotective in animal models of the disease. Dihydropyridines have been safely used for decades to treat hypertension and other cardiovascular disorders. A phase II clinical trial found that isradipine was safely tolerated by patients with Parkinson’s disease, and a phase III trial is currently underway to determine whether treatment with isradipine is neuroprotective and therefore able to slow the progression of Parkinson’s disease. This manuscript reviews the current information about the use of dihydropyridines as therapy for Parkinson’s disease and discusses the possible mechanism of action of these drugs, highlighting Ca
V
1.3 calcium channels as a potential therapeutic target for neuroprotection in Parkinson’s disease. |
| doi_str_mv | 10.1007/s40263-016-0393-9 |
| format | Article |
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V
1.3 subtype calcium channels in the pathogenesis of the disorder, and drugs with some selectivity for this ion channel (brain-penetrant dihydropyridine calcium channel blockers) are neuroprotective in animal models of the disease. Dihydropyridines have been safely used for decades to treat hypertension and other cardiovascular disorders. A phase II clinical trial found that isradipine was safely tolerated by patients with Parkinson’s disease, and a phase III trial is currently underway to determine whether treatment with isradipine is neuroprotective and therefore able to slow the progression of Parkinson’s disease. This manuscript reviews the current information about the use of dihydropyridines as therapy for Parkinson’s disease and discusses the possible mechanism of action of these drugs, highlighting Ca
V
1.3 calcium channels as a potential therapeutic target for neuroprotection in Parkinson’s disease.</description><identifier>ISSN: 1172-7047</identifier><identifier>EISSN: 1179-1934</identifier><identifier>DOI: 10.1007/s40263-016-0393-9</identifier><identifier>PMID: 27826740</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Alzheimer's disease ; Animals ; Calcium ; Calcium Channel Blockers - pharmacology ; Calcium Channel Blockers - therapeutic use ; Calcium Channels - metabolism ; Clinical trials ; Clinical Trials, Phase II as Topic ; Clinical Trials, Phase III as Topic ; Conflicts of interest ; Disease Progression ; Funding ; Homeostasis ; Humans ; Hypertension ; Isradipine - pharmacology ; Isradipine - therapeutic use ; Leading Article ; Ligands ; Medicine ; Medicine & Public Health ; Mutation ; Neurodegeneration ; Neurology ; Neurons ; Neuropathology ; Neuroprotective Agents - pharmacology ; Neuroprotective Agents - therapeutic use ; Neurosciences ; Oxidative stress ; Parkinson Disease - drug therapy ; Parkinson Disease - metabolism ; Parkinson's disease ; Pharmacotherapy ; Proteins ; Psychiatry ; Psychopharmacology ; Rodents</subject><ispartof>CNS drugs, 2016-12, Vol.30 (12), p.1127-1135</ispartof><rights>Springer International Publishing Switzerland 2016</rights><rights>Copyright Springer Science & Business Media Dec 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c514t-88346907dda93aaeaf8808a057817812ad7c11f573a7e28fa92c282fdba720f23</citedby><cites>FETCH-LOGICAL-c514t-88346907dda93aaeaf8808a057817812ad7c11f573a7e28fa92c282fdba720f23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s40263-016-0393-9$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s40263-016-0393-9$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27826740$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Swart, Tara</creatorcontrib><creatorcontrib>Hurley, Michael J.</creatorcontrib><title>Calcium Channel Antagonists as Disease-Modifying Therapy for Parkinson’s Disease: Therapeutic Rationale and Current Status</title><title>CNS drugs</title><addtitle>CNS Drugs</addtitle><addtitle>CNS Drugs</addtitle><description>Parkinson’s disease is a disabling hypokinetic neurological movement disorder in which the aetiology is unknown in the majority of cases. Current pharmacological treatments, though effective at restoring movement, are only symptomatic and do nothing to slow disease progression. Electrophysiological, epidemiological and neuropathological studies have implicated Ca
V
1.3 subtype calcium channels in the pathogenesis of the disorder, and drugs with some selectivity for this ion channel (brain-penetrant dihydropyridine calcium channel blockers) are neuroprotective in animal models of the disease. Dihydropyridines have been safely used for decades to treat hypertension and other cardiovascular disorders. A phase II clinical trial found that isradipine was safely tolerated by patients with Parkinson’s disease, and a phase III trial is currently underway to determine whether treatment with isradipine is neuroprotective and therefore able to slow the progression of Parkinson’s disease. This manuscript reviews the current information about the use of dihydropyridines as therapy for Parkinson’s disease and discusses the possible mechanism of action of these drugs, highlighting Ca
V
1.3 calcium channels as a potential therapeutic target for neuroprotection in Parkinson’s disease.</description><subject>Alzheimer's disease</subject><subject>Animals</subject><subject>Calcium</subject><subject>Calcium Channel Blockers - pharmacology</subject><subject>Calcium Channel Blockers - therapeutic use</subject><subject>Calcium Channels - metabolism</subject><subject>Clinical trials</subject><subject>Clinical Trials, Phase II as Topic</subject><subject>Clinical Trials, Phase III as Topic</subject><subject>Conflicts of interest</subject><subject>Disease Progression</subject><subject>Funding</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Isradipine - pharmacology</subject><subject>Isradipine - therapeutic use</subject><subject>Leading Article</subject><subject>Ligands</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mutation</subject><subject>Neurodegeneration</subject><subject>Neurology</subject><subject>Neurons</subject><subject>Neuropathology</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Neuroprotective Agents - therapeutic use</subject><subject>Neurosciences</subject><subject>Oxidative stress</subject><subject>Parkinson Disease - drug therapy</subject><subject>Parkinson Disease - metabolism</subject><subject>Parkinson's disease</subject><subject>Pharmacotherapy</subject><subject>Proteins</subject><subject>Psychiatry</subject><subject>Psychopharmacology</subject><subject>Rodents</subject><issn>1172-7047</issn><issn>1179-1934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkc-KFDEQh4Mo7rr6AF4k4MVLtJJ0dxJvS_sXVhRdz6G2O5nN2pPMJt2HAQ--hq_nk5hxxkUEQQhUIF_9KsVHyEMOTzmAelYaEJ1kwDsG0khmbpFjzpVh3Mjm9q-7YAoadUTulXIFAI3survkSCgtOtXAMfna4zSEZU37S4zRTfQ0zrhKMZS5UCz0RSgOi2Pv0hj8NsQVPb90GTdb6lOmHzB_CbGk-OPb9xv2-QFxyxwG-hHnkCJOjmIcab_k7OJMP804L-U-ueNxKu7BoZ6Qz69envdv2Nn712_70zM2tLyZmday6QyocUQjER16rUEjtErzegSOauDct0qickJ7NGIQWvjxApUAL-QJebLP3eR0vbgy23Uog5smjC4txXLdQg1qDfwHKg0HzQ2v6OO_0Ku05Lrqjuqgk_XLu9l8Tw05lZKdt5sc1pi3loPdWbR7i7ZatDuL1tSeR4fk5WLtxpuO39oqIPZAqU9x5fIfo_-Z-hMBQahf</recordid><startdate>20161201</startdate><enddate>20161201</enddate><creator>Swart, Tara</creator><creator>Hurley, Michael J.</creator><general>Springer International Publishing</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>4T-</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20161201</creationdate><title>Calcium Channel Antagonists as Disease-Modifying Therapy for Parkinson’s Disease: Therapeutic Rationale and Current Status</title><author>Swart, Tara ; Hurley, Michael J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c514t-88346907dda93aaeaf8808a057817812ad7c11f573a7e28fa92c282fdba720f23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Alzheimer's disease</topic><topic>Animals</topic><topic>Calcium</topic><topic>Calcium Channel Blockers - pharmacology</topic><topic>Calcium Channel Blockers - therapeutic use</topic><topic>Calcium Channels - metabolism</topic><topic>Clinical trials</topic><topic>Clinical Trials, Phase II as Topic</topic><topic>Clinical Trials, Phase III as Topic</topic><topic>Conflicts of interest</topic><topic>Disease Progression</topic><topic>Funding</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Hypertension</topic><topic>Isradipine - pharmacology</topic><topic>Isradipine - therapeutic use</topic><topic>Leading Article</topic><topic>Ligands</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mutation</topic><topic>Neurodegeneration</topic><topic>Neurology</topic><topic>Neurons</topic><topic>Neuropathology</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Neuroprotective Agents - therapeutic use</topic><topic>Neurosciences</topic><topic>Oxidative stress</topic><topic>Parkinson Disease - drug therapy</topic><topic>Parkinson Disease - metabolism</topic><topic>Parkinson's disease</topic><topic>Pharmacotherapy</topic><topic>Proteins</topic><topic>Psychiatry</topic><topic>Psychopharmacology</topic><topic>Rodents</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Swart, Tara</creatorcontrib><creatorcontrib>Hurley, Michael J.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Docstoc</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Psychology</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>CNS drugs</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Swart, Tara</au><au>Hurley, Michael J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Calcium Channel Antagonists as Disease-Modifying Therapy for Parkinson’s Disease: Therapeutic Rationale and Current Status</atitle><jtitle>CNS drugs</jtitle><stitle>CNS Drugs</stitle><addtitle>CNS Drugs</addtitle><date>2016-12-01</date><risdate>2016</risdate><volume>30</volume><issue>12</issue><spage>1127</spage><epage>1135</epage><pages>1127-1135</pages><issn>1172-7047</issn><eissn>1179-1934</eissn><abstract>Parkinson’s disease is a disabling hypokinetic neurological movement disorder in which the aetiology is unknown in the majority of cases. Current pharmacological treatments, though effective at restoring movement, are only symptomatic and do nothing to slow disease progression. Electrophysiological, epidemiological and neuropathological studies have implicated Ca
V
1.3 subtype calcium channels in the pathogenesis of the disorder, and drugs with some selectivity for this ion channel (brain-penetrant dihydropyridine calcium channel blockers) are neuroprotective in animal models of the disease. Dihydropyridines have been safely used for decades to treat hypertension and other cardiovascular disorders. A phase II clinical trial found that isradipine was safely tolerated by patients with Parkinson’s disease, and a phase III trial is currently underway to determine whether treatment with isradipine is neuroprotective and therefore able to slow the progression of Parkinson’s disease. This manuscript reviews the current information about the use of dihydropyridines as therapy for Parkinson’s disease and discusses the possible mechanism of action of these drugs, highlighting Ca
V
1.3 calcium channels as a potential therapeutic target for neuroprotection in Parkinson’s disease.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>27826740</pmid><doi>10.1007/s40263-016-0393-9</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| issn | 1172-7047 1179-1934 |
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| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Alzheimer's disease Animals Calcium Calcium Channel Blockers - pharmacology Calcium Channel Blockers - therapeutic use Calcium Channels - metabolism Clinical trials Clinical Trials, Phase II as Topic Clinical Trials, Phase III as Topic Conflicts of interest Disease Progression Funding Homeostasis Humans Hypertension Isradipine - pharmacology Isradipine - therapeutic use Leading Article Ligands Medicine Medicine & Public Health Mutation Neurodegeneration Neurology Neurons Neuropathology Neuroprotective Agents - pharmacology Neuroprotective Agents - therapeutic use Neurosciences Oxidative stress Parkinson Disease - drug therapy Parkinson Disease - metabolism Parkinson's disease Pharmacotherapy Proteins Psychiatry Psychopharmacology Rodents |
| title | Calcium Channel Antagonists as Disease-Modifying Therapy for Parkinson’s Disease: Therapeutic Rationale and Current Status |
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