The neurobiology of zinc in health and disease
Key Points Long appreciated for its biological activity by the ancients, the zinc ion is now recognized as an important component of biological signalling cascades, with roles in practically every cell and tissue type. The role of zinc in central neuronal function and signalling is increasingly bein...
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| Veröffentlicht in: | Nature reviews. Neuroscience 2005-06, Vol.6 (6), p.449-462 |
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| description | Key Points
Long appreciated for its biological activity by the ancients, the zinc ion is now recognized as an important component of biological signalling cascades, with roles in practically every cell and tissue type. The role of zinc in central neuronal function and signalling is increasingly being appreciated. Of particular importance in both function and disease is the synaptic release of zinc from certain neurons by calcium-and impulse-dependent exocytosis. The neurons that release zinc in the mammalian cerebrum are all glutamatergic, and elaboration of the role that these neurons play in cerebral function is currently underway. The modulation of cortical excitability or 'tone' and the modulation of synaptic plasticity are two prominent theories.
'Free' (rapidly exchangeable) Zn
2+
is highly toxic. The 'safe' concentration of free zinc in the extracellular fluids of the brain is about 10 nM. Several proteins have been identified that modulate the uptake and export of zinc in all tissues, but only ZnT3 expression is unique to the brain, where it is confined to the synaptic vesicle membranes of a subset of glutamatergic fibres.
Zinc has two clear roles in brain injury and brain disease. First, neurons increase their intracellular 'free' zinc by ∼1,000–10,000-fold after excitotoxic injury (such as stroke). Buffering that free zinc back down to normal levels can rescue affected neurons from apoptotic death. Second, Zn
2+
, in tandem with oxidative damage, induces the precipitation of amyloid-β into amyloid plaques and congophilic angiopathy, the pathological hallmarks of Alzheimer's disease. Genetic ablation of ZnT3 abolishes amyloid deposition in a transgenic model of Alzheimer's disease.
Pharmacological therapies for excitotoxic brain injury and neurodegenerative brain disease based on the concept of buffering the free zinc in the brain (pZn) to the appropriate, physiological concentration (pZn ∼8) have been shown to be effective in preclinical models and are currently undergoing clinical trials. Some encouraging results have been obtained in both areas, with neuroprotection for stroke and slowed progression of symptoms in Alzheimer's disease.
Zinc signalling is also attracting attention outside the brain, where many cell types also secrete zinc. Now that the appropriate tools and techniques for imaging, quantifying and administering zinc are becoming available, research in this field is set to accelerate.
The use of zinc in medicinal skin cream was men |
| doi_str_mv | 10.1038/nrn1671 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_17846769</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A188972982</galeid><sourcerecordid>A188972982</sourcerecordid><originalsourceid>FETCH-LOGICAL-c505t-1da20e06047f2321001f43a79cb7ee84baab1d00e9b061c0c2dd030c3acffca03</originalsourceid><addsrcrecordid>eNpd0E1r3DAQBmBRWpo0KfkHwRT6cdntjOyV5GMI_YJALynkZsbyaFfBKyXS-rD59VVYk4Wgg4T0jF5phLhAWCLU5ntIAZXGN-IUG40LgMa8fVnXdyfiQ873AKhQq_fiBFemRa3NqVjebrgKPKXY-zjG9b6KrnrywVY-VBumcbepKAzV4DNT5nPxztGY-eM8n4l_P3_cXv9e3Pz99ef66mZhV7DaLXAgCQwKGu1kLbEku6Ym3dpeM5umJ-pxAOC2B4UWrBwGqMHWZJ2zBPWZ-HK49yHFx4nzrtv6bHkcKXCccofaNEqrtsBPr-B9nFIob-ukbNrWwKopaHlAaxq588HFXSJbxsBbb2Ng58v-FRrTatkaWQq-Hgpsijkndt1D8ltK-w6he254Nze8yMs5f-q3PBzd3OECPs-AsqXRJQrW56NTBpSEZ_ft4HI5CmtOx4-8zvwPUhOTfg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>224998054</pqid></control><display><type>article</type><title>The neurobiology of zinc in health and disease</title><source>MEDLINE</source><source>Nature Journals Online</source><source>SpringerLink Journals - AutoHoldings</source><creator>Frederickson, Christopher J. ; Koh, Jae-Young ; Bush, Ashley I.</creator><creatorcontrib>Frederickson, Christopher J. ; Koh, Jae-Young ; Bush, Ashley I.</creatorcontrib><description>Key Points
Long appreciated for its biological activity by the ancients, the zinc ion is now recognized as an important component of biological signalling cascades, with roles in practically every cell and tissue type. The role of zinc in central neuronal function and signalling is increasingly being appreciated. Of particular importance in both function and disease is the synaptic release of zinc from certain neurons by calcium-and impulse-dependent exocytosis. The neurons that release zinc in the mammalian cerebrum are all glutamatergic, and elaboration of the role that these neurons play in cerebral function is currently underway. The modulation of cortical excitability or 'tone' and the modulation of synaptic plasticity are two prominent theories.
'Free' (rapidly exchangeable) Zn
2+
is highly toxic. The 'safe' concentration of free zinc in the extracellular fluids of the brain is about 10 nM. Several proteins have been identified that modulate the uptake and export of zinc in all tissues, but only ZnT3 expression is unique to the brain, where it is confined to the synaptic vesicle membranes of a subset of glutamatergic fibres.
Zinc has two clear roles in brain injury and brain disease. First, neurons increase their intracellular 'free' zinc by ∼1,000–10,000-fold after excitotoxic injury (such as stroke). Buffering that free zinc back down to normal levels can rescue affected neurons from apoptotic death. Second, Zn
2+
, in tandem with oxidative damage, induces the precipitation of amyloid-β into amyloid plaques and congophilic angiopathy, the pathological hallmarks of Alzheimer's disease. Genetic ablation of ZnT3 abolishes amyloid deposition in a transgenic model of Alzheimer's disease.
Pharmacological therapies for excitotoxic brain injury and neurodegenerative brain disease based on the concept of buffering the free zinc in the brain (pZn) to the appropriate, physiological concentration (pZn ∼8) have been shown to be effective in preclinical models and are currently undergoing clinical trials. Some encouraging results have been obtained in both areas, with neuroprotection for stroke and slowed progression of symptoms in Alzheimer's disease.
Zinc signalling is also attracting attention outside the brain, where many cell types also secrete zinc. Now that the appropriate tools and techniques for imaging, quantifying and administering zinc are becoming available, research in this field is set to accelerate.
The use of zinc in medicinal skin cream was mentioned in Egyptian papyri from 2000 BC (for example, the Smith Papyrus
1
), and zinc has apparently been used fairly steadily throughout Roman
2
and modern times (for example, as the American lotion named for its zinc ore, 'Calamine'). It is, therefore, somewhat ironic that zinc is a relatively late addition to the pantheon of signal ions in biology and medicine. However, the number of biological functions, health implications and pharmacological targets that are emerging for zinc indicate that it might turn out to be 'the calcium of the twenty-first century'.</description><identifier>ISSN: 1471-003X</identifier><identifier>ISSN: 1471-0048</identifier><identifier>EISSN: 1471-0048</identifier><identifier>EISSN: 1469-3178</identifier><identifier>DOI: 10.1038/nrn1671</identifier><identifier>PMID: 15891778</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Animal Genetics and Genomics ; Animals ; Behavioral Sciences ; Biochemistry. Physiology. Immunology ; Biological and medical sciences ; Biological Techniques ; Biology ; Biomedical and Life Sciences ; Biomedicine ; Brain research ; Crustacea ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Fundamental and applied biological sciences. Psychology ; Health ; Humans ; Invertebrates ; Laboratories ; Medical sciences ; Neurobiology ; Neurobiology - trends ; Neurodegenerative Diseases - metabolism ; Neurodegenerative Diseases - prevention & control ; Neurology ; Neurons ; Neurosciences ; Oxidation ; Physiology. Development ; review-article ; Signal Transduction - physiology ; Zinc - metabolism ; Zinc - physiology ; Zinc - therapeutic use ; Zinc - toxicity</subject><ispartof>Nature reviews. Neuroscience, 2005-06, Vol.6 (6), p.449-462</ispartof><rights>Springer Nature Limited 2005</rights><rights>2006 INIST-CNRS</rights><rights>COPYRIGHT 2005 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jun 2005</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c505t-1da20e06047f2321001f43a79cb7ee84baab1d00e9b061c0c2dd030c3acffca03</citedby><cites>FETCH-LOGICAL-c505t-1da20e06047f2321001f43a79cb7ee84baab1d00e9b061c0c2dd030c3acffca03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/nrn1671$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/nrn1671$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16806208$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15891778$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Frederickson, Christopher J.</creatorcontrib><creatorcontrib>Koh, Jae-Young</creatorcontrib><creatorcontrib>Bush, Ashley I.</creatorcontrib><title>The neurobiology of zinc in health and disease</title><title>Nature reviews. Neuroscience</title><addtitle>Nat Rev Neurosci</addtitle><addtitle>Nat Rev Neurosci</addtitle><description>Key Points
Long appreciated for its biological activity by the ancients, the zinc ion is now recognized as an important component of biological signalling cascades, with roles in practically every cell and tissue type. The role of zinc in central neuronal function and signalling is increasingly being appreciated. Of particular importance in both function and disease is the synaptic release of zinc from certain neurons by calcium-and impulse-dependent exocytosis. The neurons that release zinc in the mammalian cerebrum are all glutamatergic, and elaboration of the role that these neurons play in cerebral function is currently underway. The modulation of cortical excitability or 'tone' and the modulation of synaptic plasticity are two prominent theories.
'Free' (rapidly exchangeable) Zn
2+
is highly toxic. The 'safe' concentration of free zinc in the extracellular fluids of the brain is about 10 nM. Several proteins have been identified that modulate the uptake and export of zinc in all tissues, but only ZnT3 expression is unique to the brain, where it is confined to the synaptic vesicle membranes of a subset of glutamatergic fibres.
Zinc has two clear roles in brain injury and brain disease. First, neurons increase their intracellular 'free' zinc by ∼1,000–10,000-fold after excitotoxic injury (such as stroke). Buffering that free zinc back down to normal levels can rescue affected neurons from apoptotic death. Second, Zn
2+
, in tandem with oxidative damage, induces the precipitation of amyloid-β into amyloid plaques and congophilic angiopathy, the pathological hallmarks of Alzheimer's disease. Genetic ablation of ZnT3 abolishes amyloid deposition in a transgenic model of Alzheimer's disease.
Pharmacological therapies for excitotoxic brain injury and neurodegenerative brain disease based on the concept of buffering the free zinc in the brain (pZn) to the appropriate, physiological concentration (pZn ∼8) have been shown to be effective in preclinical models and are currently undergoing clinical trials. Some encouraging results have been obtained in both areas, with neuroprotection for stroke and slowed progression of symptoms in Alzheimer's disease.
Zinc signalling is also attracting attention outside the brain, where many cell types also secrete zinc. Now that the appropriate tools and techniques for imaging, quantifying and administering zinc are becoming available, research in this field is set to accelerate.
The use of zinc in medicinal skin cream was mentioned in Egyptian papyri from 2000 BC (for example, the Smith Papyrus
1
), and zinc has apparently been used fairly steadily throughout Roman
2
and modern times (for example, as the American lotion named for its zinc ore, 'Calamine'). It is, therefore, somewhat ironic that zinc is a relatively late addition to the pantheon of signal ions in biology and medicine. However, the number of biological functions, health implications and pharmacological targets that are emerging for zinc indicate that it might turn out to be 'the calcium of the twenty-first century'.</description><subject>Animal Genetics and Genomics</subject><subject>Animals</subject><subject>Behavioral Sciences</subject><subject>Biochemistry. Physiology. Immunology</subject><subject>Biological and medical sciences</subject><subject>Biological Techniques</subject><subject>Biology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain research</subject><subject>Crustacea</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Health</subject><subject>Humans</subject><subject>Invertebrates</subject><subject>Laboratories</subject><subject>Medical sciences</subject><subject>Neurobiology</subject><subject>Neurobiology - trends</subject><subject>Neurodegenerative Diseases - metabolism</subject><subject>Neurodegenerative Diseases - prevention & control</subject><subject>Neurology</subject><subject>Neurons</subject><subject>Neurosciences</subject><subject>Oxidation</subject><subject>Physiology. Development</subject><subject>review-article</subject><subject>Signal Transduction - physiology</subject><subject>Zinc - metabolism</subject><subject>Zinc - physiology</subject><subject>Zinc - therapeutic use</subject><subject>Zinc - toxicity</subject><issn>1471-003X</issn><issn>1471-0048</issn><issn>1471-0048</issn><issn>1469-3178</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpd0E1r3DAQBmBRWpo0KfkHwRT6cdntjOyV5GMI_YJALynkZsbyaFfBKyXS-rD59VVYk4Wgg4T0jF5phLhAWCLU5ntIAZXGN-IUG40LgMa8fVnXdyfiQ873AKhQq_fiBFemRa3NqVjebrgKPKXY-zjG9b6KrnrywVY-VBumcbepKAzV4DNT5nPxztGY-eM8n4l_P3_cXv9e3Pz99ef66mZhV7DaLXAgCQwKGu1kLbEku6Ym3dpeM5umJ-pxAOC2B4UWrBwGqMHWZJ2zBPWZ-HK49yHFx4nzrtv6bHkcKXCccofaNEqrtsBPr-B9nFIob-ukbNrWwKopaHlAaxq588HFXSJbxsBbb2Ng58v-FRrTatkaWQq-Hgpsijkndt1D8ltK-w6he254Nze8yMs5f-q3PBzd3OECPs-AsqXRJQrW56NTBpSEZ_ft4HI5CmtOx4-8zvwPUhOTfg</recordid><startdate>20050601</startdate><enddate>20050601</enddate><creator>Frederickson, Christopher J.</creator><creator>Koh, Jae-Young</creator><creator>Bush, Ashley I.</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>IQODW</scope><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>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7RV</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</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>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>RC3</scope></search><sort><creationdate>20050601</creationdate><title>The neurobiology of zinc in health and disease</title><author>Frederickson, Christopher J. ; Koh, Jae-Young ; Bush, Ashley I.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c505t-1da20e06047f2321001f43a79cb7ee84baab1d00e9b061c0c2dd030c3acffca03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animal Genetics and Genomics</topic><topic>Animals</topic><topic>Behavioral Sciences</topic><topic>Biochemistry. Physiology. Immunology</topic><topic>Biological and medical sciences</topic><topic>Biological Techniques</topic><topic>Biology</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain research</topic><topic>Crustacea</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Health</topic><topic>Humans</topic><topic>Invertebrates</topic><topic>Laboratories</topic><topic>Medical sciences</topic><topic>Neurobiology</topic><topic>Neurobiology - trends</topic><topic>Neurodegenerative Diseases - metabolism</topic><topic>Neurodegenerative Diseases - prevention & control</topic><topic>Neurology</topic><topic>Neurons</topic><topic>Neurosciences</topic><topic>Oxidation</topic><topic>Physiology. Development</topic><topic>review-article</topic><topic>Signal Transduction - physiology</topic><topic>Zinc - metabolism</topic><topic>Zinc - physiology</topic><topic>Zinc - therapeutic use</topic><topic>Zinc - toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Frederickson, Christopher J.</creatorcontrib><creatorcontrib>Koh, Jae-Young</creatorcontrib><creatorcontrib>Bush, Ashley I.</creatorcontrib><collection>Pascal-Francis</collection><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>Animal Behavior Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids 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>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</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>Genetics Abstracts</collection><jtitle>Nature reviews. Neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Frederickson, Christopher J.</au><au>Koh, Jae-Young</au><au>Bush, Ashley I.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The neurobiology of zinc in health and disease</atitle><jtitle>Nature reviews. Neuroscience</jtitle><stitle>Nat Rev Neurosci</stitle><addtitle>Nat Rev Neurosci</addtitle><date>2005-06-01</date><risdate>2005</risdate><volume>6</volume><issue>6</issue><spage>449</spage><epage>462</epage><pages>449-462</pages><issn>1471-003X</issn><issn>1471-0048</issn><eissn>1471-0048</eissn><eissn>1469-3178</eissn><abstract>Key Points
Long appreciated for its biological activity by the ancients, the zinc ion is now recognized as an important component of biological signalling cascades, with roles in practically every cell and tissue type. The role of zinc in central neuronal function and signalling is increasingly being appreciated. Of particular importance in both function and disease is the synaptic release of zinc from certain neurons by calcium-and impulse-dependent exocytosis. The neurons that release zinc in the mammalian cerebrum are all glutamatergic, and elaboration of the role that these neurons play in cerebral function is currently underway. The modulation of cortical excitability or 'tone' and the modulation of synaptic plasticity are two prominent theories.
'Free' (rapidly exchangeable) Zn
2+
is highly toxic. The 'safe' concentration of free zinc in the extracellular fluids of the brain is about 10 nM. Several proteins have been identified that modulate the uptake and export of zinc in all tissues, but only ZnT3 expression is unique to the brain, where it is confined to the synaptic vesicle membranes of a subset of glutamatergic fibres.
Zinc has two clear roles in brain injury and brain disease. First, neurons increase their intracellular 'free' zinc by ∼1,000–10,000-fold after excitotoxic injury (such as stroke). Buffering that free zinc back down to normal levels can rescue affected neurons from apoptotic death. Second, Zn
2+
, in tandem with oxidative damage, induces the precipitation of amyloid-β into amyloid plaques and congophilic angiopathy, the pathological hallmarks of Alzheimer's disease. Genetic ablation of ZnT3 abolishes amyloid deposition in a transgenic model of Alzheimer's disease.
Pharmacological therapies for excitotoxic brain injury and neurodegenerative brain disease based on the concept of buffering the free zinc in the brain (pZn) to the appropriate, physiological concentration (pZn ∼8) have been shown to be effective in preclinical models and are currently undergoing clinical trials. Some encouraging results have been obtained in both areas, with neuroprotection for stroke and slowed progression of symptoms in Alzheimer's disease.
Zinc signalling is also attracting attention outside the brain, where many cell types also secrete zinc. Now that the appropriate tools and techniques for imaging, quantifying and administering zinc are becoming available, research in this field is set to accelerate.
The use of zinc in medicinal skin cream was mentioned in Egyptian papyri from 2000 BC (for example, the Smith Papyrus
1
), and zinc has apparently been used fairly steadily throughout Roman
2
and modern times (for example, as the American lotion named for its zinc ore, 'Calamine'). It is, therefore, somewhat ironic that zinc is a relatively late addition to the pantheon of signal ions in biology and medicine. However, the number of biological functions, health implications and pharmacological targets that are emerging for zinc indicate that it might turn out to be 'the calcium of the twenty-first century'.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>15891778</pmid><doi>10.1038/nrn1671</doi><tpages>14</tpages></addata></record> |
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| subjects | Animal Genetics and Genomics Animals Behavioral Sciences Biochemistry. Physiology. Immunology Biological and medical sciences Biological Techniques Biology Biomedical and Life Sciences Biomedicine Brain research Crustacea Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Fundamental and applied biological sciences. Psychology Health Humans Invertebrates Laboratories Medical sciences Neurobiology Neurobiology - trends Neurodegenerative Diseases - metabolism Neurodegenerative Diseases - prevention & control Neurology Neurons Neurosciences Oxidation Physiology. Development review-article Signal Transduction - physiology Zinc - metabolism Zinc - physiology Zinc - therapeutic use Zinc - toxicity |
| title | The neurobiology of zinc in health and disease |
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