Manganese and its Role in Parkinson’s Disease: From Transport to Neuropathology
The purpose of this review is to highlight recent advances in the neuropathology associated with Mn exposures. We commence with a discussion on occupational manganism and clinical aspects of the disorder. This is followed by novel considerations on Mn transport (see also chapter by Yokel, this volum...
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| Veröffentlicht in: | Neuromolecular medicine 2009-12, Vol.11 (4), p.252-266 |
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| description | The purpose of this review is to highlight recent advances in the neuropathology associated with Mn exposures. We commence with a discussion on occupational manganism and clinical aspects of the disorder. This is followed by novel considerations on Mn transport (see also chapter by Yokel, this volume), advancing new hypotheses on the involvement of several transporters in Mn entry into the brain. This is followed by a brief description of the effects of Mn on neurotransmitter systems that are putative modulators of dopamine (DA) biology (the primary target of Mn neurotoxicity), as well as its effects on mitochondrial dysfunction and disruption of cellular energy metabolism. Next, we discuss inflammatory activation of glia in neuronal injury and how disruption of synaptic transmission and glial-neuronal communication may serve as underlying mechanisms of Mn-induced neurodegeneration commensurate with the cross-talk between glia and neurons. We conclude with a discussion on therapeutic aspects of Mn exposure. Emphasis is directed at treatment modalities and the utility of chelators in attenuating the neurodegenerative sequelae of exposure to Mn. For additional reading on several topics inherent to this review as well as others, the reader may wish to consult Aschner and Dorman (Toxicological Review 25:147–154,
2007
) and Bowman et al. (Metals and neurodegeneration,
2009
). |
| doi_str_mv | 10.1007/s12017-009-8083-0 |
| format | Article |
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2007
) and Bowman et al. (Metals and neurodegeneration,
2009
).</description><identifier>ISSN: 1535-1084</identifier><identifier>EISSN: 1559-1174</identifier><identifier>DOI: 10.1007/s12017-009-8083-0</identifier><identifier>PMID: 19657747</identifier><language>eng</language><publisher>New York: Humana Press Inc</publisher><subject>Animals ; Biological Transport ; Biomedical and Life Sciences ; Biomedicine ; Chelating Agents - therapeutic use ; Chelation Therapy ; Energy Metabolism ; Humans ; Internal Medicine ; Manganese - metabolism ; Manganese - toxicity ; Manganese Poisoning - complications ; Manganese Poisoning - drug therapy ; Manganese Poisoning - metabolism ; Manganese Poisoning - pathology ; Membrane Transport Proteins - metabolism ; Mice ; Mitochondria - metabolism ; Neurodegeneration ; Neuroglia - drug effects ; Neuroglia - metabolism ; Neuroglia - pathology ; Neurology ; Neurosciences ; Occupational Exposure ; Original Paper ; Parkinson Disease, Secondary - chemically induced ; Parkinson Disease, Secondary - metabolism ; Parkinson Disease, Secondary - pathology ; Rats ; Synaptic Transmission - drug effects</subject><ispartof>Neuromolecular medicine, 2009-12, Vol.11 (4), p.252-266</ispartof><rights>Humana Press Inc. 2009</rights><rights>Springer Science+Business Media, LLC 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c566t-757b4117887c23aafbe65d453c0da6b20c867b49119bacfb4fa4ec99e49fe2093</citedby><cites>FETCH-LOGICAL-c566t-757b4117887c23aafbe65d453c0da6b20c867b49119bacfb4fa4ec99e49fe2093</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/s12017-009-8083-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12017-009-8083-0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19657747$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Aschner, Michael</creatorcontrib><creatorcontrib>Erikson, Keith M.</creatorcontrib><creatorcontrib>Hernández, Elena Herrero</creatorcontrib><creatorcontrib>Tjalkens, Ronald</creatorcontrib><title>Manganese and its Role in Parkinson’s Disease: From Transport to Neuropathology</title><title>Neuromolecular medicine</title><addtitle>Neuromol Med</addtitle><addtitle>Neuromolecular Med</addtitle><description>The purpose of this review is to highlight recent advances in the neuropathology associated with Mn exposures. We commence with a discussion on occupational manganism and clinical aspects of the disorder. This is followed by novel considerations on Mn transport (see also chapter by Yokel, this volume), advancing new hypotheses on the involvement of several transporters in Mn entry into the brain. This is followed by a brief description of the effects of Mn on neurotransmitter systems that are putative modulators of dopamine (DA) biology (the primary target of Mn neurotoxicity), as well as its effects on mitochondrial dysfunction and disruption of cellular energy metabolism. Next, we discuss inflammatory activation of glia in neuronal injury and how disruption of synaptic transmission and glial-neuronal communication may serve as underlying mechanisms of Mn-induced neurodegeneration commensurate with the cross-talk between glia and neurons. We conclude with a discussion on therapeutic aspects of Mn exposure. Emphasis is directed at treatment modalities and the utility of chelators in attenuating the neurodegenerative sequelae of exposure to Mn. For additional reading on several topics inherent to this review as well as others, the reader may wish to consult Aschner and Dorman (Toxicological Review 25:147–154,
2007
) and Bowman et al. (Metals and neurodegeneration,
2009
).</description><subject>Animals</subject><subject>Biological Transport</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Chelating Agents - therapeutic use</subject><subject>Chelation Therapy</subject><subject>Energy Metabolism</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Manganese - metabolism</subject><subject>Manganese - toxicity</subject><subject>Manganese Poisoning - complications</subject><subject>Manganese Poisoning - drug therapy</subject><subject>Manganese Poisoning - metabolism</subject><subject>Manganese Poisoning - pathology</subject><subject>Membrane Transport Proteins - metabolism</subject><subject>Mice</subject><subject>Mitochondria - metabolism</subject><subject>Neurodegeneration</subject><subject>Neuroglia - drug effects</subject><subject>Neuroglia - metabolism</subject><subject>Neuroglia - pathology</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Occupational Exposure</subject><subject>Original Paper</subject><subject>Parkinson Disease, Secondary - chemically induced</subject><subject>Parkinson Disease, Secondary - metabolism</subject><subject>Parkinson Disease, Secondary - pathology</subject><subject>Rats</subject><subject>Synaptic Transmission - drug effects</subject><issn>1535-1084</issn><issn>1559-1174</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kcluFDEQhi0EIiHwAFyQxSWnTlzezQEpCmSRwpIonC23xz3p0GNP7G6k3PIaeT2eBE9mRACJU5VUX_21_Ai9BrIHhKj9ApSAaggxjSaaNeQJ2gYhTAOg-NNVzkQDRPMt9KKUa0IoBYDnaAuMFEpxtY3OP7k4dzGUgF2c4X4s-CINAfcRf3X5ex9Lij_v7gv-0JfgSniHj3Ja4MvsYlmmPOIx4c9hymnpxqs0pPntS_Ssc0MJrzZxB307-nh5eNKcfTk-PTw4a7yQcmyUUC2ve2qtPGXOdW2QYsYF82TmZEuJ17ISBsC0znct7xwP3pjATRcoMWwHvV_rLqd2EWY-xDG7wS5zv3D51ibX278rsb-y8_TDcglMSV0FdjcCOd1MoYx20RcfhqG-I03FKi6pEvph1Nt_yOs05Vivs1ozzqhkskKwhnxOpeTQ_V4FiF3ZZdd22WqXXdllSe158-cNjx0bfypA10CppTgP-XHy_1V_AarjofU</recordid><startdate>20091201</startdate><enddate>20091201</enddate><creator>Aschner, Michael</creator><creator>Erikson, Keith M.</creator><creator>Hernández, Elena Herrero</creator><creator>Tjalkens, Ronald</creator><general>Humana Press Inc</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>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FD</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>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>5PM</scope></search><sort><creationdate>20091201</creationdate><title>Manganese and its Role in Parkinson’s Disease: From Transport to Neuropathology</title><author>Aschner, Michael ; 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We commence with a discussion on occupational manganism and clinical aspects of the disorder. This is followed by novel considerations on Mn transport (see also chapter by Yokel, this volume), advancing new hypotheses on the involvement of several transporters in Mn entry into the brain. This is followed by a brief description of the effects of Mn on neurotransmitter systems that are putative modulators of dopamine (DA) biology (the primary target of Mn neurotoxicity), as well as its effects on mitochondrial dysfunction and disruption of cellular energy metabolism. Next, we discuss inflammatory activation of glia in neuronal injury and how disruption of synaptic transmission and glial-neuronal communication may serve as underlying mechanisms of Mn-induced neurodegeneration commensurate with the cross-talk between glia and neurons. We conclude with a discussion on therapeutic aspects of Mn exposure. Emphasis is directed at treatment modalities and the utility of chelators in attenuating the neurodegenerative sequelae of exposure to Mn. For additional reading on several topics inherent to this review as well as others, the reader may wish to consult Aschner and Dorman (Toxicological Review 25:147–154,
2007
) and Bowman et al. (Metals and neurodegeneration,
2009
).</abstract><cop>New York</cop><pub>Humana Press Inc</pub><pmid>19657747</pmid><doi>10.1007/s12017-009-8083-0</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biological Transport Biomedical and Life Sciences Biomedicine Chelating Agents - therapeutic use Chelation Therapy Energy Metabolism Humans Internal Medicine Manganese - metabolism Manganese - toxicity Manganese Poisoning - complications Manganese Poisoning - drug therapy Manganese Poisoning - metabolism Manganese Poisoning - pathology Membrane Transport Proteins - metabolism Mice Mitochondria - metabolism Neurodegeneration Neuroglia - drug effects Neuroglia - metabolism Neuroglia - pathology Neurology Neurosciences Occupational Exposure Original Paper Parkinson Disease, Secondary - chemically induced Parkinson Disease, Secondary - metabolism Parkinson Disease, Secondary - pathology Rats Synaptic Transmission - drug effects |
| title | Manganese and its Role in Parkinson’s Disease: From Transport to Neuropathology |
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