TDP-43 Pathology Progression Along the Olfactory Pathway as a Possible Substrate for Olfactory Impairment in Amyotrophic Lateral Sclerosis.
Identifieur interne : 000342 ( PubMed/Curation ); précédent : 000341; suivant : 000343TDP-43 Pathology Progression Along the Olfactory Pathway as a Possible Substrate for Olfactory Impairment in Amyotrophic Lateral Sclerosis.
Auteurs : Takahiro Takeda ; Mutsumi Iijima ; Toshiki Uchihara ; Takashi Ohashi ; Danielle Seilhean ; Charles Duyckaerts ; Shinichiro UchiyamaSource :
- Journal of neuropathology and experimental neurology [ 1554-6578 ] ; 2015.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Amyotrophic Lateral Sclerosis (complications), Analysis of Variance, Cognition Disorders (etiology), DNA-Binding Proteins (metabolism), Disease Progression, Female, Hippocampus (metabolism), Humans, Male, Middle Aged, Olfaction Disorders (etiology), Olfaction Disorders (pathology), Olfactory Cortex (metabolism), Statistics, Nonparametric.
- MESH :
- chemical , metabolism : DNA-Binding Proteins.
- complications : Amyotrophic Lateral Sclerosis.
- etiology : Cognition Disorders, Olfaction Disorders.
- metabolism : Hippocampus, Olfactory Cortex.
- pathology : Olfaction Disorders.
- Aged, Aged, 80 and over, Analysis of Variance, Disease Progression, Female, Humans, Male, Middle Aged, Statistics, Nonparametric.
Abstract
Odor impairment and its relationship with TAR DNA-binding protein 43 (TDP-43) pathology in patients with amyotrophic lateral sclerosis (ALS) have not been fully elucidated. We performed the odor stick identification test for Japanese (OSIT-J) in 18 ALS patients and in 18 controls. The score was significantly decreased (6.6 ± 2.7) in the patients versus the controls (9.2 ± 2.4) (U = 77.0, p = 0.007). This decrement of the OSIT-J score paralleled the cognitive decline. We then studied samples from a series of 42 postmortem ALS cases. Quantitative analyses demonstrated that TDP-43-positive inclusions were most frequent in the hippocampus and least abundant in the olfactory bulb and were of intermediate density in the primary olfactory cortex. This centrifugal gradient suggests that TDP-43 pathology starts in the hippocampus, spreads into the primary olfactory center, and finally reaches the olfactory bulb. TDP-43, tau, and α-synuclein accumulations appeared to be independent. These observations suggest that impaired odor discrimination in ALS patients may be related to TDP-43-positive lesions affecting predominantly secondary olfactory centers (especially the hippocampus) in contrast to decreased odor sensitivity in Parkinson disease in which α-synuclein pathology mainly involves the peripheral region (i.e., olfactory bulb). We suggest that detectable odor impairments in ALS patients are useful for predicting the presence of TDP-43 pathology in the extramotor system.
DOI: 10.1097/NEN.0000000000000198
PubMed: 25933387
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Takahiro Takeda<affiliation><nlm:affiliation>From the Department of Neurology, Tokyo Women's Medical University (TT, MI, SU); Laboratory of Structural Neuropathology, Tokyo Metropolitan Institute of Medical Science (TT, TU); Department of Neurology, Tokyo Women's Medical University Yachiyo Medical Center, Tokyo, Japan (TO); and Raymond Escourolle Laboratory of Neuropathology, Université Pierre et Marie Curie, Assistance Publique-Hôpitaux de Paris, La Salpêtrière Hospital, Paris, France (TT, DS, CD).</nlm:affiliation><wicri:noCountry code="subField">CD)</wicri:noCountry></affiliation>Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">TDP-43 Pathology Progression Along the Olfactory Pathway as a Possible Substrate for Olfactory Impairment in Amyotrophic Lateral Sclerosis.</title><author><name sortKey="Takeda, Takahiro" sort="Takeda, Takahiro" uniqKey="Takeda T" first="Takahiro" last="Takeda">Takahiro Takeda</name><affiliation><nlm:affiliation>From the Department of Neurology, Tokyo Women's Medical University (TT, MI, SU); Laboratory of Structural Neuropathology, Tokyo Metropolitan Institute of Medical Science (TT, TU); Department of Neurology, Tokyo Women's Medical University Yachiyo Medical Center, Tokyo, Japan (TO); and Raymond Escourolle Laboratory of Neuropathology, Université Pierre et Marie Curie, Assistance Publique-Hôpitaux de Paris, La Salpêtrière Hospital, Paris, France (TT, DS, CD).</nlm:affiliation><wicri:noCountry code="subField">CD)</wicri:noCountry></affiliation></author><author><name sortKey="Iijima, Mutsumi" sort="Iijima, Mutsumi" uniqKey="Iijima M" first="Mutsumi" last="Iijima">Mutsumi Iijima</name></author><author><name sortKey="Uchihara, Toshiki" sort="Uchihara, Toshiki" uniqKey="Uchihara T" first="Toshiki" last="Uchihara">Toshiki Uchihara</name></author><author><name sortKey="Ohashi, Takashi" sort="Ohashi, Takashi" uniqKey="Ohashi T" first="Takashi" last="Ohashi">Takashi Ohashi</name></author><author><name sortKey="Seilhean, Danielle" sort="Seilhean, Danielle" uniqKey="Seilhean D" first="Danielle" last="Seilhean">Danielle Seilhean</name></author><author><name sortKey="Duyckaerts, Charles" sort="Duyckaerts, Charles" uniqKey="Duyckaerts C" first="Charles" last="Duyckaerts">Charles Duyckaerts</name></author><author><name sortKey="Uchiyama, Shinichiro" sort="Uchiyama, Shinichiro" uniqKey="Uchiyama S" first="Shinichiro" last="Uchiyama">Shinichiro Uchiyama</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2015">2015</date><idno type="RBID">pubmed:25933387</idno><idno type="pmid">25933387</idno><idno type="doi">10.1097/NEN.0000000000000198</idno><idno type="wicri:Area/PubMed/Corpus">000344</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000344</idno><idno type="wicri:Area/PubMed/Curation">000342</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000342</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">TDP-43 Pathology Progression Along the Olfactory Pathway as a Possible Substrate for Olfactory Impairment in Amyotrophic Lateral Sclerosis.</title><author><name sortKey="Takeda, Takahiro" sort="Takeda, Takahiro" uniqKey="Takeda T" first="Takahiro" last="Takeda">Takahiro Takeda</name><affiliation><nlm:affiliation>From the Department of Neurology, Tokyo Women's Medical University (TT, MI, SU); Laboratory of Structural Neuropathology, Tokyo Metropolitan Institute of Medical Science (TT, TU); Department of Neurology, Tokyo Women's Medical University Yachiyo Medical Center, Tokyo, Japan (TO); and Raymond Escourolle Laboratory of Neuropathology, Université Pierre et Marie Curie, Assistance Publique-Hôpitaux de Paris, La Salpêtrière Hospital, Paris, France (TT, DS, CD).</nlm:affiliation><wicri:noCountry code="subField">CD)</wicri:noCountry></affiliation></author><author><name sortKey="Iijima, Mutsumi" sort="Iijima, Mutsumi" uniqKey="Iijima M" first="Mutsumi" last="Iijima">Mutsumi Iijima</name></author><author><name sortKey="Uchihara, Toshiki" sort="Uchihara, Toshiki" uniqKey="Uchihara T" first="Toshiki" last="Uchihara">Toshiki Uchihara</name></author><author><name sortKey="Ohashi, Takashi" sort="Ohashi, Takashi" uniqKey="Ohashi T" first="Takashi" last="Ohashi">Takashi Ohashi</name></author><author><name sortKey="Seilhean, Danielle" sort="Seilhean, Danielle" uniqKey="Seilhean D" first="Danielle" last="Seilhean">Danielle Seilhean</name></author><author><name sortKey="Duyckaerts, Charles" sort="Duyckaerts, Charles" uniqKey="Duyckaerts C" first="Charles" last="Duyckaerts">Charles Duyckaerts</name></author><author><name sortKey="Uchiyama, Shinichiro" sort="Uchiyama, Shinichiro" uniqKey="Uchiyama S" first="Shinichiro" last="Uchiyama">Shinichiro Uchiyama</name></author></analytic><series><title level="j">Journal of neuropathology and experimental neurology</title><idno type="eISSN">1554-6578</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Amyotrophic Lateral Sclerosis (complications)</term><term>Analysis of Variance</term><term>Cognition Disorders (etiology)</term><term>DNA-Binding Proteins (metabolism)</term><term>Disease Progression</term><term>Female</term><term>Hippocampus (metabolism)</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Olfaction Disorders (etiology)</term><term>Olfaction Disorders (pathology)</term><term>Olfactory Cortex (metabolism)</term><term>Statistics, Nonparametric</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>DNA-Binding Proteins</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Amyotrophic Lateral Sclerosis</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Cognition Disorders</term><term>Olfaction Disorders</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Hippocampus</term><term>Olfactory Cortex</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Olfaction Disorders</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Analysis of Variance</term><term>Disease Progression</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Statistics, Nonparametric</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Odor impairment and its relationship with TAR DNA-binding protein 43 (TDP-43) pathology in patients with amyotrophic lateral sclerosis (ALS) have not been fully elucidated. We performed the odor stick identification test for Japanese (OSIT-J) in 18 ALS patients and in 18 controls. The score was significantly decreased (6.6 ± 2.7) in the patients versus the controls (9.2 ± 2.4) (U = 77.0, p = 0.007). This decrement of the OSIT-J score paralleled the cognitive decline. We then studied samples from a series of 42 postmortem ALS cases. Quantitative analyses demonstrated that TDP-43-positive inclusions were most frequent in the hippocampus and least abundant in the olfactory bulb and were of intermediate density in the primary olfactory cortex. This centrifugal gradient suggests that TDP-43 pathology starts in the hippocampus, spreads into the primary olfactory center, and finally reaches the olfactory bulb. TDP-43, tau, and α-synuclein accumulations appeared to be independent. These observations suggest that impaired odor discrimination in ALS patients may be related to TDP-43-positive lesions affecting predominantly secondary olfactory centers (especially the hippocampus) in contrast to decreased odor sensitivity in Parkinson disease in which α-synuclein pathology mainly involves the peripheral region (i.e., olfactory bulb). We suggest that detectable odor impairments in ALS patients are useful for predicting the presence of TDP-43 pathology in the extramotor system.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25933387</PMID><DateCreated><Year>2015</Year><Month>05</Month><Day>18</Day></DateCreated><DateCompleted><Year>2015</Year><Month>07</Month><Day>27</Day></DateCompleted><DateRevised><Year>2015</Year><Month>05</Month><Day>18</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1554-6578</ISSN><JournalIssue CitedMedium="Internet"><Volume>74</Volume><Issue>6</Issue><PubDate><Year>2015</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Journal of neuropathology and experimental neurology</Title><ISOAbbreviation>J. Neuropathol. Exp. Neurol.</ISOAbbreviation></Journal><ArticleTitle>TDP-43 Pathology Progression Along the Olfactory Pathway as a Possible Substrate for Olfactory Impairment in Amyotrophic Lateral Sclerosis.</ArticleTitle><Pagination><MedlinePgn>547-56</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1097/NEN.0000000000000198</ELocationID><Abstract><AbstractText>Odor impairment and its relationship with TAR DNA-binding protein 43 (TDP-43) pathology in patients with amyotrophic lateral sclerosis (ALS) have not been fully elucidated. We performed the odor stick identification test for Japanese (OSIT-J) in 18 ALS patients and in 18 controls. The score was significantly decreased (6.6 ± 2.7) in the patients versus the controls (9.2 ± 2.4) (U = 77.0, p = 0.007). This decrement of the OSIT-J score paralleled the cognitive decline. We then studied samples from a series of 42 postmortem ALS cases. Quantitative analyses demonstrated that TDP-43-positive inclusions were most frequent in the hippocampus and least abundant in the olfactory bulb and were of intermediate density in the primary olfactory cortex. This centrifugal gradient suggests that TDP-43 pathology starts in the hippocampus, spreads into the primary olfactory center, and finally reaches the olfactory bulb. TDP-43, tau, and α-synuclein accumulations appeared to be independent. These observations suggest that impaired odor discrimination in ALS patients may be related to TDP-43-positive lesions affecting predominantly secondary olfactory centers (especially the hippocampus) in contrast to decreased odor sensitivity in Parkinson disease in which α-synuclein pathology mainly involves the peripheral region (i.e., olfactory bulb). We suggest that detectable odor impairments in ALS patients are useful for predicting the presence of TDP-43 pathology in the extramotor system.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Takeda</LastName><ForeName>Takahiro</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>From the Department of Neurology, Tokyo Women's Medical University (TT, MI, SU); Laboratory of Structural Neuropathology, Tokyo Metropolitan Institute of Medical Science (TT, TU); Department of Neurology, Tokyo Women's Medical University Yachiyo Medical Center, Tokyo, Japan (TO); and Raymond Escourolle Laboratory of Neuropathology, Université Pierre et Marie Curie, Assistance Publique-Hôpitaux de Paris, La Salpêtrière Hospital, Paris, France (TT, DS, CD).</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Iijima</LastName><ForeName>Mutsumi</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Uchihara</LastName><ForeName>Toshiki</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Ohashi</LastName><ForeName>Takashi</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Seilhean</LastName><ForeName>Danielle</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Duyckaerts</LastName><ForeName>Charles</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Uchiyama</LastName><ForeName>Shinichiro</ForeName><Initials>S</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Neuropathol Exp Neurol</MedlineTA><NlmUniqueID>2985192R</NlmUniqueID><ISSNLinking>0022-3069</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004268">DNA-Binding Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C000598624">TDP-43 protein, human</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000369" MajorTopicYN="N">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000690" MajorTopicYN="N">Amyotrophic Lateral Sclerosis</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000704" MajorTopicYN="N">Analysis of Variance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003072" MajorTopicYN="N">Cognition Disorders</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004268" MajorTopicYN="N">DNA-Binding Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018450" MajorTopicYN="N">Disease Progression</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006624" MajorTopicYN="N">Hippocampus</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000857" MajorTopicYN="N">Olfaction Disorders</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D066194" MajorTopicYN="N">Olfactory Cortex</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018709" MajorTopicYN="N">Statistics, Nonparametric</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>5</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>5</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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