Comparison of extent of tau pathology in patients with frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP-17), frontotemporal lobar degeneration with Pick bodies and early onset Alzheimer's disease
In order to gain insight into the pathogenesis of frontotemporal lobar degeneration (FTLD), the mean tau load in frontal cortex was compared in 34 patients with frontotemporal dementia linked to chromosome 17 (FTDP‐17) with 12 different mutations in the tau gene (MAPT), 11 patients with sporadic FTL...
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| creator | Shiarli, A.-M. Jennings, R. Shi, J. Bailey, K. Davidson, Y. Tian, J. Bigio, E. H. Ghetti, B. Murrell, J. R. Delisle, M. B. Mirra, S. Crain, B. Zolo, P. Arima, K. Iseki, E. Murayama, S. Kretzschmar, H. Neumann, M. Lippa, C. Halliday, G. MacKenzie, J. Khan, N. Ravid, R. Dickson, D. Wszolek, Z. Iwatsubo, T. Pickering-Brown, S. M. Mann, D. M. A. |
| description | In order to gain insight into the pathogenesis of frontotemporal lobar degeneration (FTLD), the mean tau load in frontal cortex was compared in 34 patients with frontotemporal dementia linked to chromosome 17 (FTDP‐17) with 12 different mutations in the tau gene (MAPT), 11 patients with sporadic FTLD with Pick bodies and 25 patients with early onset Alzheimer’s disease (EOAD). Tau load was determined, as percentage of tissue occupied by stained product, by image analysis of immunohistochemically stained sections using the phospho‐dependent antibodies AT8, AT100 and AT180. With AT8 and AT180 antibodies, the amount of tau was significantly (P |
| doi_str_mv | 10.1111/j.1365-2990.2006.00736.x |
| format | Article |
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H. ; Ghetti, B. ; Murrell, J. R. ; Delisle, M. B. ; Mirra, S. ; Crain, B. ; Zolo, P. ; Arima, K. ; Iseki, E. ; Murayama, S. ; Kretzschmar, H. ; Neumann, M. ; Lippa, C. ; Halliday, G. ; MacKenzie, J. ; Khan, N. ; Ravid, R. ; Dickson, D. ; Wszolek, Z. ; Iwatsubo, T. ; Pickering-Brown, S. M. ; Mann, D. M. A.</creator><creatorcontrib>Shiarli, A.-M. ; Jennings, R. ; Shi, J. ; Bailey, K. ; Davidson, Y. ; Tian, J. ; Bigio, E. H. ; Ghetti, B. ; Murrell, J. R. ; Delisle, M. B. ; Mirra, S. ; Crain, B. ; Zolo, P. ; Arima, K. ; Iseki, E. ; Murayama, S. ; Kretzschmar, H. ; Neumann, M. ; Lippa, C. ; Halliday, G. ; MacKenzie, J. ; Khan, N. ; Ravid, R. ; Dickson, D. ; Wszolek, Z. ; Iwatsubo, T. ; Pickering-Brown, S. M. ; Mann, D. M. A.</creatorcontrib><description>In order to gain insight into the pathogenesis of frontotemporal lobar degeneration (FTLD), the mean tau load in frontal cortex was compared in 34 patients with frontotemporal dementia linked to chromosome 17 (FTDP‐17) with 12 different mutations in the tau gene (MAPT), 11 patients with sporadic FTLD with Pick bodies and 25 patients with early onset Alzheimer’s disease (EOAD). Tau load was determined, as percentage of tissue occupied by stained product, by image analysis of immunohistochemically stained sections using the phospho‐dependent antibodies AT8, AT100 and AT180. With AT8 and AT180 antibodies, the amount of tau was significantly (P < 0.001 in each instance) less than that in EOAD for both FTDP‐17 (8.5% and 10.0% respectively) and sporadic FTLD with Pick bodies (16.1% and 10.0% respectively). With AT100, the amount of tau detected in FTDP‐17 was 54% (P < 0.001) of that detected in EOAD, but no tau was detected in sporadic FTLD with Pick bodies using this particular antibody. The amount of insoluble tau deposited within the brain in FTDP‐17 did not depend in any systematic way upon where the MAPT mutation was topographically located within the gene, or on the physiological or structural change generated by the mutation, regardless of which anti‐tau antibody was used. Not only does the amount of tau deposited in the brain differ between the three disorders, but the pattern of phosphorylation of tau also varies according to disease. These findings raise important questions relating to the role of aggregated tau in neurodegeneration – whether this represents an adaptive response which promotes the survival of neurones, or whether it is a detrimental change that directly, or indirectly, brings about the demize of the affected cell.</description><identifier>ISSN: 0305-1846</identifier><identifier>EISSN: 1365-2990</identifier><identifier>DOI: 10.1111/j.1365-2990.2006.00736.x</identifier><identifier>PMID: 16866983</identifier><identifier>CODEN: NANEDL</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adult ; Age of Onset ; Aged ; Alzheimer Disease - genetics ; Alzheimer Disease - pathology ; Alzheimer's disease ; Apolipoproteins E - genetics ; Biological and medical sciences ; Brain - pathology ; Chromosomes, Human, Pair 17 ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Dementia - genetics ; Dementia - pathology ; Female ; frontotemporal lobar degeneration ; Genotype ; Human viral diseases ; Humans ; Image Processing, Computer-Assisted ; Immunohistochemistry ; Infectious diseases ; Male ; Medical sciences ; Microtubule-Associated Proteins - genetics ; Middle Aged ; Nerve Tissue Proteins - genetics ; neurofibrillary tangle ; Neurology ; Parkinsonian Disorders - genetics ; Parkinsonian Disorders - pathology ; Pick bodies ; Pick Disease of the Brain - genetics ; Pick Disease of the Brain - pathology ; Tau gene ; Tau protein ; tau Proteins - metabolism ; Viral diseases ; Viral diseases of the nervous system</subject><ispartof>Neuropathology and applied neurobiology, 2006-08, Vol.32 (4), p.374-387</ispartof><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4656-792f55c9f045729c2f24b7f7ea77aa5606d4317bd4a59545ca5b7cb8bb36abea3</citedby><cites>FETCH-LOGICAL-c4656-792f55c9f045729c2f24b7f7ea77aa5606d4317bd4a59545ca5b7cb8bb36abea3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1365-2990.2006.00736.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1365-2990.2006.00736.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1416,27922,27923,45572,45573</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17941251$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16866983$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shiarli, A.-M.</creatorcontrib><creatorcontrib>Jennings, R.</creatorcontrib><creatorcontrib>Shi, J.</creatorcontrib><creatorcontrib>Bailey, K.</creatorcontrib><creatorcontrib>Davidson, Y.</creatorcontrib><creatorcontrib>Tian, J.</creatorcontrib><creatorcontrib>Bigio, E. H.</creatorcontrib><creatorcontrib>Ghetti, B.</creatorcontrib><creatorcontrib>Murrell, J. R.</creatorcontrib><creatorcontrib>Delisle, M. B.</creatorcontrib><creatorcontrib>Mirra, S.</creatorcontrib><creatorcontrib>Crain, B.</creatorcontrib><creatorcontrib>Zolo, P.</creatorcontrib><creatorcontrib>Arima, K.</creatorcontrib><creatorcontrib>Iseki, E.</creatorcontrib><creatorcontrib>Murayama, S.</creatorcontrib><creatorcontrib>Kretzschmar, H.</creatorcontrib><creatorcontrib>Neumann, M.</creatorcontrib><creatorcontrib>Lippa, C.</creatorcontrib><creatorcontrib>Halliday, G.</creatorcontrib><creatorcontrib>MacKenzie, J.</creatorcontrib><creatorcontrib>Khan, N.</creatorcontrib><creatorcontrib>Ravid, R.</creatorcontrib><creatorcontrib>Dickson, D.</creatorcontrib><creatorcontrib>Wszolek, Z.</creatorcontrib><creatorcontrib>Iwatsubo, T.</creatorcontrib><creatorcontrib>Pickering-Brown, S. M.</creatorcontrib><creatorcontrib>Mann, D. M. A.</creatorcontrib><title>Comparison of extent of tau pathology in patients with frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP-17), frontotemporal lobar degeneration with Pick bodies and early onset Alzheimer's disease</title><title>Neuropathology and applied neurobiology</title><addtitle>Neuropathol Appl Neurobiol</addtitle><description>In order to gain insight into the pathogenesis of frontotemporal lobar degeneration (FTLD), the mean tau load in frontal cortex was compared in 34 patients with frontotemporal dementia linked to chromosome 17 (FTDP‐17) with 12 different mutations in the tau gene (MAPT), 11 patients with sporadic FTLD with Pick bodies and 25 patients with early onset Alzheimer’s disease (EOAD). Tau load was determined, as percentage of tissue occupied by stained product, by image analysis of immunohistochemically stained sections using the phospho‐dependent antibodies AT8, AT100 and AT180. With AT8 and AT180 antibodies, the amount of tau was significantly (P < 0.001 in each instance) less than that in EOAD for both FTDP‐17 (8.5% and 10.0% respectively) and sporadic FTLD with Pick bodies (16.1% and 10.0% respectively). With AT100, the amount of tau detected in FTDP‐17 was 54% (P < 0.001) of that detected in EOAD, but no tau was detected in sporadic FTLD with Pick bodies using this particular antibody. The amount of insoluble tau deposited within the brain in FTDP‐17 did not depend in any systematic way upon where the MAPT mutation was topographically located within the gene, or on the physiological or structural change generated by the mutation, regardless of which anti‐tau antibody was used. Not only does the amount of tau deposited in the brain differ between the three disorders, but the pattern of phosphorylation of tau also varies according to disease. These findings raise important questions relating to the role of aggregated tau in neurodegeneration – whether this represents an adaptive response which promotes the survival of neurones, or whether it is a detrimental change that directly, or indirectly, brings about the demize of the affected cell.</description><subject>Adult</subject><subject>Age of Onset</subject><subject>Aged</subject><subject>Alzheimer Disease - genetics</subject><subject>Alzheimer Disease - pathology</subject><subject>Alzheimer's disease</subject><subject>Apolipoproteins E - genetics</subject><subject>Biological and medical sciences</subject><subject>Brain - pathology</subject><subject>Chromosomes, Human, Pair 17</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Dementia - genetics</subject><subject>Dementia - pathology</subject><subject>Female</subject><subject>frontotemporal lobar degeneration</subject><subject>Genotype</subject><subject>Human viral diseases</subject><subject>Humans</subject><subject>Image Processing, Computer-Assisted</subject><subject>Immunohistochemistry</subject><subject>Infectious diseases</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Microtubule-Associated Proteins - genetics</subject><subject>Middle Aged</subject><subject>Nerve Tissue Proteins - genetics</subject><subject>neurofibrillary tangle</subject><subject>Neurology</subject><subject>Parkinsonian Disorders - genetics</subject><subject>Parkinsonian Disorders - pathology</subject><subject>Pick bodies</subject><subject>Pick Disease of the Brain - genetics</subject><subject>Pick Disease of the Brain - pathology</subject><subject>Tau gene</subject><subject>Tau protein</subject><subject>tau Proteins - metabolism</subject><subject>Viral diseases</subject><subject>Viral diseases of the nervous system</subject><issn>0305-1846</issn><issn>1365-2990</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNUs2O0zAQjhCILQuvgHzhTyLFTmI7kfZSFbaAqrKHRUhcrEky2bp14mKn2pZH5WlwSLUrcQFfbOv7mdHMF0WE0SkL591mylLB46Qo6DShVEwplamYHh5EkzvgYTShKeUxyzNxFj3xfkMp5VIUj6MzJnIhijydRL_mtt2B0952xDYEDz12_fDqYU920K-tsTdHorvhowPmya3u16Rxtuttj-3OOjCkxjZgGkbwCtxWd8FS-5YY3W2xJr0l1drZ1nrbImGSvL68fn8VM_nm7d9mxpbgguUNduhC1dDaaKurLSltrdET6GqC4MyR2M5jT2bm5xp1i-6VJ7X2CB6fRo8aMB6fne7z6Ovlh-v5x3j5ZfFpPlvGVSa4iGWRNJxXRUMzLpOiSpokK2UjEaQE4IKKOkuZLOsMeMEzXgEvZVXmZZkKKBHS8-jl6Ltz9scefa9a7Ss0Bjq0e6_CrGXOhfwnkRVZmudpHoj5SKyc9d5ho3ZOt-COilE1BEBt1LBnNexZDQFQfwKgDkH6_FRjX7ZY3wtPGw-EFycC-ApM46CrtL_nySJjCWeBdzHybrXB4383oFazVXgEeTzKte_xcCcPwVBhEpKrb6uFWsjvnC0pVZ_T39DC36E</recordid><startdate>200608</startdate><enddate>200608</enddate><creator>Shiarli, A.-M.</creator><creator>Jennings, R.</creator><creator>Shi, J.</creator><creator>Bailey, K.</creator><creator>Davidson, Y.</creator><creator>Tian, J.</creator><creator>Bigio, E. 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A.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell Science</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>200608</creationdate><title>Comparison of extent of tau pathology in patients with frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP-17), frontotemporal lobar degeneration with Pick bodies and early onset Alzheimer's disease</title><author>Shiarli, A.-M. ; Jennings, R. ; Shi, J. ; Bailey, K. ; Davidson, Y. ; Tian, J. ; Bigio, E. H. ; Ghetti, B. ; Murrell, J. R. ; Delisle, M. B. ; Mirra, S. ; Crain, B. ; Zolo, P. ; Arima, K. ; Iseki, E. ; Murayama, S. ; Kretzschmar, H. ; Neumann, M. ; Lippa, C. ; Halliday, G. ; MacKenzie, J. ; Khan, N. ; Ravid, R. ; Dickson, D. ; Wszolek, Z. ; Iwatsubo, T. ; Pickering-Brown, S. M. ; Mann, D. M. A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4656-792f55c9f045729c2f24b7f7ea77aa5606d4317bd4a59545ca5b7cb8bb36abea3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adult</topic><topic>Age of Onset</topic><topic>Aged</topic><topic>Alzheimer Disease - genetics</topic><topic>Alzheimer Disease - pathology</topic><topic>Alzheimer's disease</topic><topic>Apolipoproteins E - genetics</topic><topic>Biological and medical sciences</topic><topic>Brain - pathology</topic><topic>Chromosomes, Human, Pair 17</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. 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Tau load was determined, as percentage of tissue occupied by stained product, by image analysis of immunohistochemically stained sections using the phospho‐dependent antibodies AT8, AT100 and AT180. With AT8 and AT180 antibodies, the amount of tau was significantly (P < 0.001 in each instance) less than that in EOAD for both FTDP‐17 (8.5% and 10.0% respectively) and sporadic FTLD with Pick bodies (16.1% and 10.0% respectively). With AT100, the amount of tau detected in FTDP‐17 was 54% (P < 0.001) of that detected in EOAD, but no tau was detected in sporadic FTLD with Pick bodies using this particular antibody. The amount of insoluble tau deposited within the brain in FTDP‐17 did not depend in any systematic way upon where the MAPT mutation was topographically located within the gene, or on the physiological or structural change generated by the mutation, regardless of which anti‐tau antibody was used. Not only does the amount of tau deposited in the brain differ between the three disorders, but the pattern of phosphorylation of tau also varies according to disease. These findings raise important questions relating to the role of aggregated tau in neurodegeneration – whether this represents an adaptive response which promotes the survival of neurones, or whether it is a detrimental change that directly, or indirectly, brings about the demize of the affected cell.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>16866983</pmid><doi>10.1111/j.1365-2990.2006.00736.x</doi><tpages>14</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0305-1846 |
| ispartof | Neuropathology and applied neurobiology, 2006-08, Vol.32 (4), p.374-387 |
| issn | 0305-1846 1365-2990 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_68678567 |
| source | Wiley-Blackwell Journals; MEDLINE |
| subjects | Adult Age of Onset Aged Alzheimer Disease - genetics Alzheimer Disease - pathology Alzheimer's disease Apolipoproteins E - genetics Biological and medical sciences Brain - pathology Chromosomes, Human, Pair 17 Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Dementia - genetics Dementia - pathology Female frontotemporal lobar degeneration Genotype Human viral diseases Humans Image Processing, Computer-Assisted Immunohistochemistry Infectious diseases Male Medical sciences Microtubule-Associated Proteins - genetics Middle Aged Nerve Tissue Proteins - genetics neurofibrillary tangle Neurology Parkinsonian Disorders - genetics Parkinsonian Disorders - pathology Pick bodies Pick Disease of the Brain - genetics Pick Disease of the Brain - pathology Tau gene Tau protein tau Proteins - metabolism Viral diseases Viral diseases of the nervous system |
| title | Comparison of extent of tau pathology in patients with frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP-17), frontotemporal lobar degeneration with Pick bodies and early onset Alzheimer's disease |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-14T15%3A21%3A35IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Comparison%20of%20extent%20of%20tau%20pathology%20in%20patients%20with%20frontotemporal%20dementia%20with%20Parkinsonism%20linked%20to%20chromosome%2017%20(FTDP-17),%20frontotemporal%20lobar%20degeneration%20with%20Pick%20bodies%20and%20early%20onset%20Alzheimer's%20disease&rft.jtitle=Neuropathology%20and%20applied%20neurobiology&rft.au=Shiarli,%20A.-M.&rft.date=2006-08&rft.volume=32&rft.issue=4&rft.spage=374&rft.epage=387&rft.pages=374-387&rft.issn=0305-1846&rft.eissn=1365-2990&rft.coden=NANEDL&rft_id=info:doi/10.1111/j.1365-2990.2006.00736.x&rft_dat=%3Cproquest_cross%3E68678567%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=19438838&rft_id=info:pmid/16866983&rfr_iscdi=true |