Proton magnetic resonance spectroscopy in Huntington's disease: Evidence in favour of the glutamate excitotoxic theory?
Identifieur interne : 005591 ( Main/Exploration ); précédent : 005590; suivant : 005592Proton magnetic resonance spectroscopy in Huntington's disease: Evidence in favour of the glutamate excitotoxic theory?
Auteurs : Taylor‐Robinson [Royaume-Uni] ; R. A. Weeks [Royaume-Uni] ; D. J. Bryant [Royaume-Uni] ; J. Sargentoni [Royaume-Uni] ; C. D. Marcus [Royaume-Uni] ; A. E. Harding [Royaume-Uni] ; D. J. Brooks [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 1996-03.
English descriptors
- KwdEn :
- Aspartic Acid (analogs & derivatives), Aspartic Acid (physiology), Cerebral Cortex (physiopathology), Corpus Striatum (pathology), Corpus Striatum (physiopathology), Excitotoxicity, Glutamic Acid (physiology), Glutamine, Glutamine (physiology), Gultamate, Heterozygote Detection, Humans, Huntington Disease (diagnosis), Huntington Disease (genetics), Huntington Disease (physiopathology), Huntington's disease, Magnetic Resonance Imaging, Nerve Degeneration (genetics), Nerve Degeneration (physiology), Proton magnetic resonance spectroscopy, Reference Values, Synaptic Transmission (physiology).
- MESH :
- chemical , analogs & derivatives : Aspartic Acid.
- chemical , physiology : Aspartic Acid, Glutamic Acid, Glutamine.
- diagnosis : Huntington Disease.
- genetics : Huntington Disease, Nerve Degeneration.
- pathology : Corpus Striatum.
- physiology : Nerve Degeneration, Synaptic Transmission.
- physiopathology : Cerebral Cortex, Corpus Striatum, Huntington Disease.
- Heterozygote Detection, Humans, Magnetic Resonance Imaging, Reference Values.
Abstract
The gene responsible for Huntington's disease (HD) has been located, but its action and the pathophysiology of HD remain unclear. Glutamate excitotoxicity may contribute to the striatal neurodegeneration seen in HD. We used localised proton magnetic resonance spectroscopy (MRS) of the brain to investigate five patients with early HD, one symptom‐free gene carrier, and 14 healthy volunteers. Peak area ratios of choline‐containing compounds (Cho), glutamine and glutamate (Glx), and N‐acetyl moieties including N‐acetylaspartate (NAx), relative to creatine (Cr), were calculated. Spectra were analysed from the striatum and the occipital and the temporal cortex. The HD patients all had an elevated Glx/Cr in spectra localised to the striatum, compared with healthy controls, and one patient also had an elevated thalamic Glx/Cr. The mean Glx/Cr was unaltered in the cortical spectra of HD patients. The asymptomatic gene carrier displayed no spectral abnormalities. Our findings suggest disordered striatal glutamate metabolism and may support the theory of glutamate excitotoxicity in HD.
Url:
DOI: 10.1002/mds.870110209
Affiliations:
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A." last="Weeks">R. A. Weeks</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Department of Neurology, London</wicri:cityArea></affiliation></author><author><name sortKey="Bryant, D J" sort="Bryant, D J" uniqKey="Bryant D" first="D. J." last="Bryant">D. J. Bryant</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>The Robert Steiner MR Unit, London</wicri:cityArea></affiliation></author><author><name sortKey="Sargentoni, J" sort="Sargentoni, J" uniqKey="Sargentoni J" first="J." last="Sargentoni">J. Sargentoni</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>The Robert Steiner MR Unit, London</wicri:cityArea></affiliation></author><author><name sortKey="Marcus, C D" sort="Marcus, C D" uniqKey="Marcus C" first="C. D." last="Marcus">C. D. Marcus</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>The Robert Steiner MR Unit, London</wicri:cityArea></affiliation></author><author><name sortKey="Harding, A E" sort="Harding, A E" uniqKey="Harding A" first="A. E." last="Harding">A. E. Harding</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Institute of Neurology, London</wicri:cityArea></affiliation></author><author><name sortKey="Brooks, D J" sort="Brooks, D J" uniqKey="Brooks D" first="D. J." last="Brooks">D. J. Brooks</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Department of Neurology, London</wicri:cityArea></affiliation><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Institute of Neurology, London</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1996-03">1996-03</date><biblScope unit="vol">11</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="167">167</biblScope><biblScope unit="page" to="173">173</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">4F623389AB366DBB310349F060326843B67A6F42</idno><idno type="DOI">10.1002/mds.870110209</idno><idno type="ArticleID">MDS870110209</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aspartic Acid (analogs & derivatives)</term><term>Aspartic Acid (physiology)</term><term>Cerebral Cortex (physiopathology)</term><term>Corpus Striatum (pathology)</term><term>Corpus Striatum (physiopathology)</term><term>Excitotoxicity</term><term>Glutamic Acid (physiology)</term><term>Glutamine</term><term>Glutamine (physiology)</term><term>Gultamate</term><term>Heterozygote Detection</term><term>Humans</term><term>Huntington Disease (diagnosis)</term><term>Huntington Disease (genetics)</term><term>Huntington Disease (physiopathology)</term><term>Huntington's disease</term><term>Magnetic Resonance Imaging</term><term>Nerve Degeneration (genetics)</term><term>Nerve Degeneration (physiology)</term><term>Proton magnetic resonance spectroscopy</term><term>Reference Values</term><term>Synaptic Transmission (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Aspartic Acid</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Aspartic Acid</term><term>Glutamic Acid</term><term>Glutamine</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Huntington Disease</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Huntington Disease</term><term>Nerve Degeneration</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Corpus Striatum</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Nerve Degeneration</term><term>Synaptic Transmission</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Cerebral Cortex</term><term>Corpus Striatum</term><term>Huntington Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Heterozygote Detection</term><term>Humans</term><term>Magnetic Resonance Imaging</term><term>Reference Values</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The gene responsible for Huntington's disease (HD) has been located, but its action and the pathophysiology of HD remain unclear. Glutamate excitotoxicity may contribute to the striatal neurodegeneration seen in HD. We used localised proton magnetic resonance spectroscopy (MRS) of the brain to investigate five patients with early HD, one symptom‐free gene carrier, and 14 healthy volunteers. Peak area ratios of choline‐containing compounds (Cho), glutamine and glutamate (Glx), and N‐acetyl moieties including N‐acetylaspartate (NAx), relative to creatine (Cr), were calculated. Spectra were analysed from the striatum and the occipital and the temporal cortex. The HD patients all had an elevated Glx/Cr in spectra localised to the striatum, compared with healthy controls, and one patient also had an elevated thalamic Glx/Cr. The mean Glx/Cr was unaltered in the cortical spectra of HD patients. The asymptomatic gene carrier displayed no spectral abnormalities. Our findings suggest disordered striatal glutamate metabolism and may support the theory of glutamate excitotoxicity in HD.</div></front></TEI><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Angleterre</li></region></list><tree><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Taylor Obinson" sort="Taylor Obinson" uniqKey="Taylor Obinson" last="Taylor-Robinson">Taylor‐Robinson</name></region><name sortKey="Brooks, D J" sort="Brooks, D J" uniqKey="Brooks D" first="D. J." last="Brooks">D. J. Brooks</name><name sortKey="Brooks, D J" sort="Brooks, D J" uniqKey="Brooks D" first="D. J." last="Brooks">D. J. Brooks</name><name sortKey="Bryant, D J" sort="Bryant, D J" uniqKey="Bryant D" first="D. J." last="Bryant">D. J. Bryant</name><name sortKey="Harding, A E" sort="Harding, A E" uniqKey="Harding A" first="A. E." last="Harding">A. E. Harding</name><name sortKey="Marcus, C D" sort="Marcus, C D" uniqKey="Marcus C" first="C. D." last="Marcus">C. D. Marcus</name><name sortKey="Sargentoni, J" sort="Sargentoni, J" uniqKey="Sargentoni J" first="J." last="Sargentoni">J. Sargentoni</name><name sortKey="Taylor Obinson" sort="Taylor Obinson" uniqKey="Taylor Obinson" last="Taylor-Robinson">Taylor‐Robinson</name><name sortKey="Weeks, R A" sort="Weeks, R A" uniqKey="Weeks R" first="R. A." last="Weeks">R. A. Weeks</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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