Regional susceptibilities to mitochondrial dysfunctions in the CNS
Identifieur interne : 000473 ( Main/Corpus ); précédent : 000472; suivant : 000474Regional susceptibilities to mitochondrial dysfunctions in the CNS
Auteurs : Milena Pinto ; Alicia M. Pickrell ; Carlos T. MoraesSource :
- Biological Chemistry [ 1431-6730 ] ; 2012-03-01.
Abstract
Mitochondrial dysfunctions are very common features of age-related neurological diseases such as Parkinson’s, Alzheimer’s and Huntington’s disease. Several studies have shown that bioenergetic impairments have a major role in the degeneration of the central nervous system (CNS) in these patients. Accordingly, one of the main symptoms in many mitochondrial diseases is severe encephalopathy. The heterogeneity of the brain in terms of anatomic structures, cell composition, regional functions and biochemical properties makes the analysis on this organ very complex and difficult to interpret. Humans, in addition to animal models, exposed to toxins that affect mitochondrial function, in particular oxidative phosphorylation, exhibit degeneration of specific regions within the brain. Moreover, mutations in ubiquitously expressed genes that are involved in mitochondrial function also induce regional-specific cell death in the CNS. In this review, we will discuss some current hypotheses to explain the regional susceptibilities to mitochondrial dysfunctions in the CNS.
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DOI: 10.1515/hsz-2011-0236
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Several studies have shown that bioenergetic impairments have a major role in the degeneration of the central nervous system (CNS) in these patients. Accordingly, one of the main symptoms in many mitochondrial diseases is severe encephalopathy. The heterogeneity of the brain in terms of anatomic structures, cell composition, regional functions and biochemical properties makes the analysis on this organ very complex and difficult to interpret. Humans, in addition to animal models, exposed to toxins that affect mitochondrial function, in particular oxidative phosphorylation, exhibit degeneration of specific regions within the brain. Moreover, mutations in ubiquitously expressed genes that are involved in mitochondrial function also induce regional-specific cell death in the CNS. In this review, we will discuss some current hypotheses to explain the regional susceptibilities to mitochondrial dysfunctions in the CNS.</p></abstract><kwd-group><title>Keywords</title><kwd>Alzheimer’s</kwd><x>, </x><kwd>Huntington’s</kwd><x>, </x><kwd>mitochondria</kwd><x>, </x><kwd>neurodegeneration</kwd><x>, </x><kwd>Parkinson’s</kwd></kwd-group><counts><fig-count count="2"></fig-count><table-count count="0"></table-count><ref-count count="45"></ref-count></counts></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Regional susceptibilities to mitochondrial dysfunctions in the CNS</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Regional susceptibilities to mitochondrial dysfunctions in the CNS</title></titleInfo><name type="personal"><namePart type="given">Milena</namePart><namePart type="family">Pinto</namePart><affiliation>Department of Neurology, University of Miami: Miller School of Medicine, Miami, FL 33136, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alicia M.</namePart><namePart type="family">Pickrell</namePart><affiliation>Neuroscience Graduate Program, University of Miami: Miller School of Medicine, Miami, FL 33136, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Carlos T.</namePart><namePart type="family">Moraes</namePart><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="review-article"></genre><originInfo><publisher>Walter de Gruyter</publisher><dateIssued encoding="w3cdtf">2012-03-01</dateIssued><copyrightDate encoding="w3cdtf">2012</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">2</extent><extent unit="references">45</extent></physicalDescription><abstract lang="en">Mitochondrial dysfunctions are very common features of age-related neurological diseases such as Parkinson’s, Alzheimer’s and Huntington’s disease. Several studies have shown that bioenergetic impairments have a major role in the degeneration of the central nervous system (CNS) in these patients. Accordingly, one of the main symptoms in many mitochondrial diseases is severe encephalopathy. The heterogeneity of the brain in terms of anatomic structures, cell composition, regional functions and biochemical properties makes the analysis on this organ very complex and difficult to interpret. Humans, in addition to animal models, exposed to toxins that affect mitochondrial function, in particular oxidative phosphorylation, exhibit degeneration of specific regions within the brain. Moreover, mutations in ubiquitously expressed genes that are involved in mitochondrial function also induce regional-specific cell death in the CNS. In this review, we will discuss some current hypotheses to explain the regional susceptibilities to mitochondrial dysfunctions in the CNS.</abstract><note type="author-notes">Corresponding author</note><subject><genre>Keywords</genre><topic>Alzheimer’s</topic><topic>Huntington’s</topic><topic>mitochondria</topic><topic>neurodegeneration</topic><topic>Parkinson’s</topic></subject><relatedItem type="host"><titleInfo><title>Biological Chemistry</title></titleInfo><titleInfo type="abbreviated"><title>Biological Chemistry</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">1431-6730</identifier><identifier type="eISSN">1437-4315</identifier><identifier type="PublisherID">bchm</identifier><part><date>2012</date><detail type="volume"><caption>vol.</caption><number>393</number></detail><detail type="issue"><caption>no.</caption><number>4</number></detail><extent unit="pages"><start>275</start><end>281</end></extent></part></relatedItem><relatedItem type="reviewOf"><genre>pdf</genre><identifier type="pdf">hsz-2011-0236.pdf</identifier></relatedItem><identifier type="istex">9EF750D78CCA00FBC23F23C814048CB9C9A7724A</identifier><identifier type="DOI">10.1515/hsz-2011-0236</identifier><identifier type="ArticleID">hsz-2011-0236</identifier><identifier type="Related-article-Href">hsz-2011-0236.pdf</identifier><accessCondition type="use and reproduction" contentType="copyright">©2012 by Walter de Gruyter Berlin Boston</accessCondition><recordInfo><recordContentSource>De Gruyter</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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