The prion hypothesis in Parkinson's disease: Braak to the future.
Identifieur interne : 000917 ( PubMed/Corpus ); précédent : 000916; suivant : 000918The prion hypothesis in Parkinson's disease: Braak to the future.
Auteurs : Naomi P. Visanji ; Patricia L. Brooks ; Lili-Naz Hazrati ; Anthony E. LangSource :
- Acta neuropathologica communications [ 2051-5960 ] ; 2013.
English descriptors
- KwdEn :
- MESH :
- chemical , physiology : Prions.
- etiology : Parkinson Disease.
- pathology : Parkinson Disease.
- physiopathology : Parkinson Disease.
- Animals, Humans, Models, Neurological, Severity of Illness Index.
Abstract
Parkinson's disease (PD) is a progressive neurodegenerative disorder typified by the presence of intraneuronal inclusions containing aggregated alpha synuclein (αsyn). The progression of parkinsonian pathology and clinical phenotype has been broadly demonstrated to follow a specific pattern, most notably described by Braak and colleagues. In more recent times it has been hypothesized that αsyn itself may be a critical factor in mediating transmission of disease pathology from one brain area to another. Here we investigate the growing body of evidence demonstrating the ability of αsyn to spread transcellularly and induce pathological aggregation affecting neurons by permissive templating and provide a critical analysis of some irregularities in the hypothesis that the progression of PD pathology may be mediated by such a prion-like process. Finally we discuss some key questions that remain unanswered which are vital to determining the potential contribution of a prion-like process to the pathogenesis of PD.
DOI: 10.1186/2051-5960-1-2
PubMed: 24252164
Links to Exploration step
pubmed:24252164Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">The prion hypothesis in Parkinson's disease: Braak to the future.</title><author><name sortKey="Visanji, Naomi P" sort="Visanji, Naomi P" uniqKey="Visanji N" first="Naomi P" last="Visanji">Naomi P. Visanji</name><affiliation><nlm:affiliation>Division of Patient Based Clinical Research, Toronto Western Research Institute, and the Edmond J, Safra Program in Parkinson's Disease, Toronto Western Hospital, McLaughlin Pavilion, 7th Floor Rm 7-403, 399 Bathurst Street, Toronto, Ontario M5T 2S8, Canada. lang@uhnres.utoronto.ca.</nlm:affiliation></affiliation></author><author><name sortKey="Brooks, Patricia L" sort="Brooks, Patricia L" uniqKey="Brooks P" first="Patricia L" last="Brooks">Patricia L. Brooks</name></author><author><name sortKey="Hazrati, Lili Naz" sort="Hazrati, Lili Naz" uniqKey="Hazrati L" first="Lili-Naz" last="Hazrati">Lili-Naz Hazrati</name></author><author><name sortKey="Lang, Anthony E" sort="Lang, Anthony E" uniqKey="Lang A" first="Anthony E" last="Lang">Anthony E. Lang</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2013">2013</date><idno type="RBID">pubmed:24252164</idno><idno type="pmid">24252164</idno><idno type="doi">10.1186/2051-5960-1-2</idno><idno type="wicri:Area/PubMed/Corpus">000917</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000917</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">The prion hypothesis in Parkinson's disease: Braak to the future.</title><author><name sortKey="Visanji, Naomi P" sort="Visanji, Naomi P" uniqKey="Visanji N" first="Naomi P" last="Visanji">Naomi P. Visanji</name><affiliation><nlm:affiliation>Division of Patient Based Clinical Research, Toronto Western Research Institute, and the Edmond J, Safra Program in Parkinson's Disease, Toronto Western Hospital, McLaughlin Pavilion, 7th Floor Rm 7-403, 399 Bathurst Street, Toronto, Ontario M5T 2S8, Canada. lang@uhnres.utoronto.ca.</nlm:affiliation></affiliation></author><author><name sortKey="Brooks, Patricia L" sort="Brooks, Patricia L" uniqKey="Brooks P" first="Patricia L" last="Brooks">Patricia L. Brooks</name></author><author><name sortKey="Hazrati, Lili Naz" sort="Hazrati, Lili Naz" uniqKey="Hazrati L" first="Lili-Naz" last="Hazrati">Lili-Naz Hazrati</name></author><author><name sortKey="Lang, Anthony E" sort="Lang, Anthony E" uniqKey="Lang A" first="Anthony E" last="Lang">Anthony E. Lang</name></author></analytic><series><title level="j">Acta neuropathologica communications</title><idno type="eISSN">2051-5960</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Humans</term><term>Models, Neurological</term><term>Parkinson Disease (etiology)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (physiopathology)</term><term>Prions (physiology)</term><term>Severity of Illness Index</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Prions</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term><term>Models, Neurological</term><term>Severity of Illness Index</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is a progressive neurodegenerative disorder typified by the presence of intraneuronal inclusions containing aggregated alpha synuclein (αsyn). The progression of parkinsonian pathology and clinical phenotype has been broadly demonstrated to follow a specific pattern, most notably described by Braak and colleagues. In more recent times it has been hypothesized that αsyn itself may be a critical factor in mediating transmission of disease pathology from one brain area to another. Here we investigate the growing body of evidence demonstrating the ability of αsyn to spread transcellularly and induce pathological aggregation affecting neurons by permissive templating and provide a critical analysis of some irregularities in the hypothesis that the progression of PD pathology may be mediated by such a prion-like process. Finally we discuss some key questions that remain unanswered which are vital to determining the potential contribution of a prion-like process to the pathogenesis of PD.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24252164</PMID><DateCreated><Year>2013</Year><Month>11</Month><Day>22</Day></DateCreated><DateCompleted><Year>2015</Year><Month>03</Month><Day>31</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2051-5960</ISSN><JournalIssue CitedMedium="Internet"><Volume>1</Volume><PubDate><Year>2013</Year><Month>May</Month><Day>08</Day></PubDate></JournalIssue><Title>Acta neuropathologica communications</Title><ISOAbbreviation>Acta Neuropathol Commun</ISOAbbreviation></Journal><ArticleTitle>The prion hypothesis in Parkinson's disease: Braak to the future.</ArticleTitle><Pagination><MedlinePgn>2</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1186/2051-5960-1-2</ELocationID><Abstract><AbstractText>Parkinson's disease (PD) is a progressive neurodegenerative disorder typified by the presence of intraneuronal inclusions containing aggregated alpha synuclein (αsyn). The progression of parkinsonian pathology and clinical phenotype has been broadly demonstrated to follow a specific pattern, most notably described by Braak and colleagues. In more recent times it has been hypothesized that αsyn itself may be a critical factor in mediating transmission of disease pathology from one brain area to another. Here we investigate the growing body of evidence demonstrating the ability of αsyn to spread transcellularly and induce pathological aggregation affecting neurons by permissive templating and provide a critical analysis of some irregularities in the hypothesis that the progression of PD pathology may be mediated by such a prion-like process. Finally we discuss some key questions that remain unanswered which are vital to determining the potential contribution of a prion-like process to the pathogenesis of PD.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Visanji</LastName><ForeName>Naomi P</ForeName><Initials>NP</Initials><AffiliationInfo><Affiliation>Division of Patient Based Clinical Research, Toronto Western Research Institute, and the Edmond J, Safra Program in Parkinson's Disease, Toronto Western Hospital, McLaughlin Pavilion, 7th Floor Rm 7-403, 399 Bathurst Street, Toronto, Ontario M5T 2S8, Canada. lang@uhnres.utoronto.ca.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Brooks</LastName><ForeName>Patricia L</ForeName><Initials>PL</Initials></Author><Author ValidYN="Y"><LastName>Hazrati</LastName><ForeName>Lili-Naz</ForeName><Initials>LN</Initials></Author><Author ValidYN="Y"><LastName>Lang</LastName><ForeName>Anthony E</ForeName><Initials>AE</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2013</Year><Month>05</Month><Day>08</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Acta Neuropathol Commun</MedlineTA><NlmUniqueID>101610673</NlmUniqueID><ISSNLinking>2051-5960</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011328">Prions</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2011 May;26(6):1042-8</RefSource><PMID Version="1">21626549</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Int J Biochem Cell Biol. 2008;40(9):1835-49</RefSource><PMID 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