La maladie de Parkinson au Canada (serveur d'exploration)

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Postmortem brain fatty acid profile of levodopa-treated Parkinson disease patients and parkinsonian monkeys

Identifieur interne : 002914 ( Main/Exploration ); précédent : 002913; suivant : 002915

Postmortem brain fatty acid profile of levodopa-treated Parkinson disease patients and parkinsonian monkeys

Auteurs : Carl Julien [Canada] ; Line Berthiaume [Canada] ; Abdallah Hadj-Tahar [Canada] ; Ali H. Rajput [Canada] ; Paul J. Bedard [Canada] ; Thérèse Di Paolo [Canada] ; Pierre Julien [Canada] ; Frédéric Calon [Canada]

Source :

RBID : Pascal:06-0205655

Descripteurs français

English descriptors

Abstract

Fatty acids play a critical role in brain function but their specific role in the pathophysiology of Parkinson disease (PD) and levodopa-induced motor complications is still unknown. From a therapeutic standpoint, it is important to determine the relation between brain fatty acids and PD because the brain fatty acid content depends on nutritional intake, a readily manipulable environmental factor. Here, we report a postmortem analysis of fatty acid profile by gas chromatography in the brain cortex of human patients (12 PD patients and nine Controls) as well as in the brain cortex of monkeys (four controls, five drug-naive MPTP monkeys and seven levodopa-treated MPTP monkeys). Brain fatty acid profile of cerebral cortex tissue was similar between PD patients and Controls and was not correlated with age of death, delay to autopsy or brain pH. Levodopa administration in MPTP monkeys increased arachidonic acid content (+7%; P < 0.05) but decreased docosahexaenoic acid concentration (-15%; P < 0.05) and total n - 3:n - 6 polyunsaturated fatty acids ratio (-27%; P < 0.01) compared to drug-naive MPTP animals. Interestingly, PD patients who experienced motor complications to levodopa had higher arachidonic acid concentrations in the cortex compared to Controls (+13.6%; P < 0.05) and to levodopa-treated PD patients devoid of motor complications (+14.4%; P < 0.05). Furthermore, PD patients who took an above-median cumulative dose of levodopa had a higher relative amount of saturated fatty acids but lower monounsaturated fatty acids in their brain cortex (P < 0.01). These results suggest that changes in brain fatty acid relative concentrations are associated with levodopa treatment in PD patients and in a non-human primate model of parkinsonism.


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<div type="abstract" xml:lang="en">Fatty acids play a critical role in brain function but their specific role in the pathophysiology of Parkinson disease (PD) and levodopa-induced motor complications is still unknown. From a therapeutic standpoint, it is important to determine the relation between brain fatty acids and PD because the brain fatty acid content depends on nutritional intake, a readily manipulable environmental factor. Here, we report a postmortem analysis of fatty acid profile by gas chromatography in the brain cortex of human patients (12 PD patients and nine Controls) as well as in the brain cortex of monkeys (four controls, five drug-naive MPTP monkeys and seven levodopa-treated MPTP monkeys). Brain fatty acid profile of cerebral cortex tissue was similar between PD patients and Controls and was not correlated with age of death, delay to autopsy or brain pH. Levodopa administration in MPTP monkeys increased arachidonic acid content (+7%; P < 0.05) but decreased docosahexaenoic acid concentration (-15%; P < 0.05) and total n - 3:n - 6 polyunsaturated fatty acids ratio (-27%; P < 0.01) compared to drug-naive MPTP animals. Interestingly, PD patients who experienced motor complications to levodopa had higher arachidonic acid concentrations in the cortex compared to Controls (+13.6%; P < 0.05) and to levodopa-treated PD patients devoid of motor complications (+14.4%; P < 0.05). Furthermore, PD patients who took an above-median cumulative dose of levodopa had a higher relative amount of saturated fatty acids but lower monounsaturated fatty acids in their brain cortex (P < 0.01). These results suggest that changes in brain fatty acid relative concentrations are associated with levodopa treatment in PD patients and in a non-human primate model of parkinsonism.</div>
</front>
</TEI>
<affiliations>
<list>
<country>
<li>Canada</li>
</country>
</list>
<tree>
<country name="Canada">
<noRegion>
<name sortKey="Julien, Carl" sort="Julien, Carl" uniqKey="Julien C" first="Carl" last="Julien">Carl Julien</name>
</noRegion>
<name sortKey="Bedard, Paul J" sort="Bedard, Paul J" uniqKey="Bedard P" first="Paul J." last="Bedard">Paul J. Bedard</name>
<name sortKey="Bedard, Paul J" sort="Bedard, Paul J" uniqKey="Bedard P" first="Paul J." last="Bedard">Paul J. Bedard</name>
<name sortKey="Berthiaume, Line" sort="Berthiaume, Line" uniqKey="Berthiaume L" first="Line" last="Berthiaume">Line Berthiaume</name>
<name sortKey="Calon, Frederic" sort="Calon, Frederic" uniqKey="Calon F" first="Frédéric" last="Calon">Frédéric Calon</name>
<name sortKey="Calon, Frederic" sort="Calon, Frederic" uniqKey="Calon F" first="Frédéric" last="Calon">Frédéric Calon</name>
<name sortKey="Di Paolo, Therese" sort="Di Paolo, Therese" uniqKey="Di Paolo T" first="Thérèse" last="Di Paolo">Thérèse Di Paolo</name>
<name sortKey="Di Paolo, Therese" sort="Di Paolo, Therese" uniqKey="Di Paolo T" first="Thérèse" last="Di Paolo">Thérèse Di Paolo</name>
<name sortKey="Hadj Tahar, Abdallah" sort="Hadj Tahar, Abdallah" uniqKey="Hadj Tahar A" first="Abdallah" last="Hadj-Tahar">Abdallah Hadj-Tahar</name>
<name sortKey="Hadj Tahar, Abdallah" sort="Hadj Tahar, Abdallah" uniqKey="Hadj Tahar A" first="Abdallah" last="Hadj-Tahar">Abdallah Hadj-Tahar</name>
<name sortKey="Julien, Carl" sort="Julien, Carl" uniqKey="Julien C" first="Carl" last="Julien">Carl Julien</name>
<name sortKey="Julien, Pierre" sort="Julien, Pierre" uniqKey="Julien P" first="Pierre" last="Julien">Pierre Julien</name>
<name sortKey="Rajput, Ali H" sort="Rajput, Ali H" uniqKey="Rajput A" first="Ali H." last="Rajput">Ali H. Rajput</name>
</country>
</tree>
</affiliations>
</record>

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