Upstream deregulation of calcium signaling in Parkinson's disease
Parkinson's disease (PD) is a major health problem affecting millions of people worldwide. Recent studies provide compelling evidence that altered Ca(2) (+) homeostasis may underlie disease pathomechanism and be an inherent feature of all vulnerable neurons. The downstream effects of altered Ca...
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| Veröffentlicht in: | Frontiers in molecular neuroscience 2014-06, Vol.7, p.53 |
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| creator | Rivero-Ríos, Pilar Gómez-Suaga, Patricia Fdez, Elena Hilfiker, Sabine |
| description | Parkinson's disease (PD) is a major health problem affecting millions of people worldwide. Recent studies provide compelling evidence that altered Ca(2) (+) homeostasis may underlie disease pathomechanism and be an inherent feature of all vulnerable neurons. The downstream effects of altered Ca(2) (+) handling in the distinct subcellular organelles for proper cellular function are beginning to be elucidated. Here, we summarize the evidence that vulnerable neurons may be exposed to homeostatic Ca(2) (+) stress which may determine their selective vulnerability, and suggest how abnormal Ca(2) (+) handling in the distinct intracellular compartments may compromise neuronal health in the context of aging, environmental, and genetic stress. Gaining a better understanding of the varied effects of Ca(2) (+) dyshomeostasis may allow novel combinatorial therapeutic strategies to slow PD progression. |
| doi_str_mv | 10.3389/fnmol.2014.00053 |
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Gaining a better understanding of the varied effects of Ca(2) (+) dyshomeostasis may allow novel combinatorial therapeutic strategies to slow PD progression.</description><identifier>ISSN: 1662-5099</identifier><identifier>EISSN: 1662-5099</identifier><identifier>DOI: 10.3389/fnmol.2014.00053</identifier><identifier>PMID: 24987329</identifier><language>eng</language><publisher>Switzerland: Frontiers Research Foundation</publisher><subject>Aging ; Apoptosis ; Calcium homeostasis ; Calcium signalling ; Deoxyribonucleic acid ; DNA ; Dopamine ; Homeostasis ; Hypotheses ; Kinases ; Mitochondria ; Mitochondrial DNA ; Movement disorders ; Neurodegenerative diseases ; Neurons ; Neuroscience ; Organelles ; Oxidative stress ; Parkinson's disease ; Proteins ; Trends</subject><ispartof>Frontiers in molecular neuroscience, 2014-06, Vol.7, p.53</ispartof><rights>2014. This work is licensed under http://creativecommons.org/licenses/by/3.0/ (the “License”). 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Recent studies provide compelling evidence that altered Ca(2) (+) homeostasis may underlie disease pathomechanism and be an inherent feature of all vulnerable neurons. The downstream effects of altered Ca(2) (+) handling in the distinct subcellular organelles for proper cellular function are beginning to be elucidated. Here, we summarize the evidence that vulnerable neurons may be exposed to homeostatic Ca(2) (+) stress which may determine their selective vulnerability, and suggest how abnormal Ca(2) (+) handling in the distinct intracellular compartments may compromise neuronal health in the context of aging, environmental, and genetic stress. Gaining a better understanding of the varied effects of Ca(2) (+) dyshomeostasis may allow novel combinatorial therapeutic strategies to slow PD progression.</description><subject>Aging</subject><subject>Apoptosis</subject><subject>Calcium homeostasis</subject><subject>Calcium signalling</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Dopamine</subject><subject>Homeostasis</subject><subject>Hypotheses</subject><subject>Kinases</subject><subject>Mitochondria</subject><subject>Mitochondrial DNA</subject><subject>Movement disorders</subject><subject>Neurodegenerative diseases</subject><subject>Neurons</subject><subject>Neuroscience</subject><subject>Organelles</subject><subject>Oxidative stress</subject><subject>Parkinson's disease</subject><subject>Proteins</subject><subject>Trends</subject><issn>1662-5099</issn><issn>1662-5099</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNpVkM1Lw0AUxBdRbK3ePUnAg6fU_c7uRZDiFxT0YM9hk7yNW5PdupsI_vcWrFJPM_CG3_AGoXOC54wpfW19H7o5xYTPMcaCHaApkZLmAmt9uOcn6CSlNcaSSsGO0YRyrQpG9RTdrjZpiGD6rIEI7diZwQWfBZvVpqvd2GfJtd50zreZ89mLie_Op-CvUta4BCbBKTqypktwttMZWt3fvS4e8-Xzw9PidplvqOZDbiwVdcULRoASBkpjrWxlbVUJ2WjDC1rUBKwBZQCzRnBVyNpADZJLRZhlM3Tzw92MVQ9NDX6Ipis30fUmfpXBuPL_xbu3sg2fJccSayG3gMsdIIaPEdJQrsMYt7-lkjKsJJOUiG3qYr_mj_87GfsGNmFwfg</recordid><startdate>20140617</startdate><enddate>20140617</enddate><creator>Rivero-Ríos, Pilar</creator><creator>Gómez-Suaga, Patricia</creator><creator>Fdez, Elena</creator><creator>Hilfiker, Sabine</creator><general>Frontiers Research Foundation</general><general>Frontiers Media S.A</general><scope>NPM</scope><scope>3V.</scope><scope>7TK</scope><scope>7XB</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>5PM</scope></search><sort><creationdate>20140617</creationdate><title>Upstream deregulation of calcium signaling in Parkinson's disease</title><author>Rivero-Ríos, Pilar ; 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Recent studies provide compelling evidence that altered Ca(2) (+) homeostasis may underlie disease pathomechanism and be an inherent feature of all vulnerable neurons. The downstream effects of altered Ca(2) (+) handling in the distinct subcellular organelles for proper cellular function are beginning to be elucidated. Here, we summarize the evidence that vulnerable neurons may be exposed to homeostatic Ca(2) (+) stress which may determine their selective vulnerability, and suggest how abnormal Ca(2) (+) handling in the distinct intracellular compartments may compromise neuronal health in the context of aging, environmental, and genetic stress. Gaining a better understanding of the varied effects of Ca(2) (+) dyshomeostasis may allow novel combinatorial therapeutic strategies to slow PD progression.</abstract><cop>Switzerland</cop><pub>Frontiers Research Foundation</pub><pmid>24987329</pmid><doi>10.3389/fnmol.2014.00053</doi><oa>free_for_read</oa></addata></record> |
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| source | PubMed (Medline); Directory of Open Access Journals; EZB Electronic Journals Library; PubMed Central Open Access |
| subjects | Aging Apoptosis Calcium homeostasis Calcium signalling Deoxyribonucleic acid DNA Dopamine Homeostasis Hypotheses Kinases Mitochondria Mitochondrial DNA Movement disorders Neurodegenerative diseases Neurons Neuroscience Organelles Oxidative stress Parkinson's disease Proteins Trends |
| title | Upstream deregulation of calcium signaling in Parkinson's disease |
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