Neuroprotective action of omega-3 polyunsaturated fatty acids against neurodegenerative diseases: evidence from animal studies.
Identifieur interne : 000843 ( Ncbi/Merge ); précédent : 000842; suivant : 000844Neuroprotective action of omega-3 polyunsaturated fatty acids against neurodegenerative diseases: evidence from animal studies.
Auteurs : Frédéric Calon [Canada] ; Greg ColeSource :
- Prostaglandins, leukotrienes, and essential fatty acids [ 0952-3278 ]
English descriptors
- KwdEn :
- Alzheimer Disease (drug therapy), Alzheimer Disease (pathology), Animals, Docosahexaenoic Acids (administration & dosage), Docosahexaenoic Acids (pharmacology), Fatty Acids, Omega-3 (administration & dosage), Fatty Acids, Omega-3 (pharmacology), Humans, Models, Biological, Neurodegenerative Diseases (drug therapy), Neurodegenerative Diseases (pathology), Neuroprotective Agents (administration & dosage), Neuroprotective Agents (pharmacology), Parkinson Disease (drug therapy), Parkinson Disease (pathology).
- MESH :
- chemical , administration & dosage : Docosahexaenoic Acids, Fatty Acids, Omega-3, Neuroprotective Agents.
- drug therapy : Alzheimer Disease, Neurodegenerative Diseases, Parkinson Disease.
- pathology : Alzheimer Disease, Neurodegenerative Diseases, Parkinson Disease.
- chemical , pharmacology : Docosahexaenoic Acids, Fatty Acids, Omega-3, Neuroprotective Agents.
- Animals, Humans, Models, Biological.
Abstract
Studies in animals clearly show that oral intake of docosahexaenoic acid (DHA) can alter brain DHA concentrations and thereby modify brain functions. This provides us with an opportunity to use DHA as a nutraceutical or pharmaceutical tool in brain disorders such as Alzheimer disease (AD) and Parkinson disease (PD). Most of the published epidemiological studies are consistent with a positive association between high reported DHA consumption or high DHA blood levels and a lower risk of developing AD later in life. Such observations have prompted the investigation of DHA in three different transgenic models of AD. These analyses show that animal models of AD are more vulnerable to DHA depletion than controls and that DHA exerts a beneficial effect against pathological signs of AD, including A beta accumulation, cognitive impairment, synaptic marker loss, and hyperphosphorylation of tau. Multiple mechanisms of action can be associated with the neuroprotective effects of DHA and include antioxidant properties and activation of distinct cell signaling pathways. Although the first randomized clinical assays have yet failed to demonstrate convincing beneficial effects of DHA for AD patients, the knowledge gathered in recent years holds out a hope for prevention and suggests that the elderly and people bearing a genetic risk for AD should at least avoid DHA deficiency.
DOI: 10.1016/j.plefa.2007.10.019
PubMed: 18037281
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This provides us with an opportunity to use DHA as a nutraceutical or pharmaceutical tool in brain disorders such as Alzheimer disease (AD) and Parkinson disease (PD). Most of the published epidemiological studies are consistent with a positive association between high reported DHA consumption or high DHA blood levels and a lower risk of developing AD later in life. Such observations have prompted the investigation of DHA in three different transgenic models of AD. These analyses show that animal models of AD are more vulnerable to DHA depletion than controls and that DHA exerts a beneficial effect against pathological signs of AD, including A beta accumulation, cognitive impairment, synaptic marker loss, and hyperphosphorylation of tau. Multiple mechanisms of action can be associated with the neuroprotective effects of DHA and include antioxidant properties and activation of distinct cell signaling pathways. Although the first randomized clinical assays have yet failed to demonstrate convincing beneficial effects of DHA for AD patients, the knowledge gathered in recent years holds out a hope for prevention and suggests that the elderly and people bearing a genetic risk for AD should at least avoid DHA deficiency.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">18037281</PMID><DateCreated><Year>2007</Year><Month>12</Month><Day>10</Day></DateCreated><DateCompleted><Year>2008</Year><Month>04</Month><Day>23</Day></DateCompleted><DateRevised><Year>2007</Year><Month>12</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0952-3278</ISSN><JournalIssue CitedMedium="Print"><Volume>77</Volume><Issue>5-6</Issue><PubDate><MedlineDate>2007 Nov-Dec</MedlineDate></PubDate></JournalIssue><Title>Prostaglandins, leukotrienes, and essential fatty acids</Title><ISOAbbreviation>Prostaglandins Leukot. Essent. Fatty Acids</ISOAbbreviation></Journal><ArticleTitle>Neuroprotective action of omega-3 polyunsaturated fatty acids against neurodegenerative diseases: evidence from animal studies.</ArticleTitle><Pagination><MedlinePgn>287-93</MedlinePgn></Pagination><Abstract><AbstractText>Studies in animals clearly show that oral intake of docosahexaenoic acid (DHA) can alter brain DHA concentrations and thereby modify brain functions. This provides us with an opportunity to use DHA as a nutraceutical or pharmaceutical tool in brain disorders such as Alzheimer disease (AD) and Parkinson disease (PD). Most of the published epidemiological studies are consistent with a positive association between high reported DHA consumption or high DHA blood levels and a lower risk of developing AD later in life. Such observations have prompted the investigation of DHA in three different transgenic models of AD. These analyses show that animal models of AD are more vulnerable to DHA depletion than controls and that DHA exerts a beneficial effect against pathological signs of AD, including A beta accumulation, cognitive impairment, synaptic marker loss, and hyperphosphorylation of tau. Multiple mechanisms of action can be associated with the neuroprotective effects of DHA and include antioxidant properties and activation of distinct cell signaling pathways. Although the first randomized clinical assays have yet failed to demonstrate convincing beneficial effects of DHA for AD patients, the knowledge gathered in recent years holds out a hope for prevention and suggests that the elderly and people bearing a genetic risk for AD should at least avoid DHA deficiency.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Calon</LastName><ForeName>Frédéric</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Molecular Endocrinology and Oncology Research Centre, Centre Hospitalier de l'Université Laval Research Centre (CHUL), 2705 Laurier Blvd, Quebec, Canada. frederic.calon@crchul.ulaval.ca</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cole</LastName><ForeName>Greg</ForeName><Initials>G</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2007</Year><Month>11</Month><Day>26</Day></ArticleDate></Article><MedlineJournalInfo><Country>Scotland</Country><MedlineTA>Prostaglandins Leukot Essent Fatty Acids</MedlineTA><NlmUniqueID>8802730</NlmUniqueID><ISSNLinking>0952-3278</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015525">Fatty Acids, Omega-3</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018696">Neuroprotective Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>25167-62-8</RegistryNumber><NameOfSubstance UI="D004281">Docosahexaenoic Acids</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000544" MajorTopicYN="N">Alzheimer Disease</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004281" MajorTopicYN="N">Docosahexaenoic Acids</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015525" MajorTopicYN="N">Fatty Acids, Omega-3</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008954" MajorTopicYN="N">Models, Biological</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019636" MajorTopicYN="N">Neurodegenerative Diseases</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018696" MajorTopicYN="N">Neuroprotective Agents</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>64</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2007</Year><Month>11</Month><Day>27</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2008</Year><Month>4</Month><Day>24</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2007</Year><Month>11</Month><Day>27</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">18037281</ArticleId><ArticleId IdType="pii">S0952-3278(07)00142-1</ArticleId><ArticleId IdType="doi">10.1016/j.plefa.2007.10.019</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li></country></list><tree><noCountry><name sortKey="Cole, Greg" sort="Cole, Greg" uniqKey="Cole G" first="Greg" last="Cole">Greg Cole</name></noCountry><country name="Canada"><noRegion><name sortKey="Calon, Frederic" sort="Calon, Frederic" uniqKey="Calon F" first="Frédéric" last="Calon">Frédéric 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