No Evidence for Shorter Leukocyte Telomere Length in Parkinson’s Disease Patients
Telomeres constitute the protective ends of chromosomes. They become shorter after each cell division, and therefore, telomere length is considered as an indicator of cellular aging. Interestingly, both inflammation and oxidative stress, which play a role in the etiology of Parkinson’s disease (PD),...
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| Veröffentlicht in: | The journals of gerontology. Series A, Biological sciences and medical sciences Biological sciences and medical sciences, 2010-11, Vol.65A (11), p.1181-1184 |
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| container_title | The journals of gerontology. Series A, Biological sciences and medical sciences |
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| creator | Eerola, Johanna Kananen, Laura Manninen, Kaisa Hellström, Olli Tienari, Pentti J. Hovatta, Iiris |
| description | Telomeres constitute the protective ends of chromosomes. They become shorter after each cell division, and therefore, telomere length is considered as an indicator of cellular aging. Interestingly, both inflammation and oxidative stress, which play a role in the etiology of Parkinson’s disease (PD), may accelerate telomere shortening. Furthermore, it has been suggested that leukocyte telomere shortening may be accelerated in PD. To replicate the earlier findings, we analyzed telomere length of peripheral blood leukocytes in a sample of 131 PD patients (aged 66.8 ± 9.7 years) and 115 controls (aged 65.4 ± 9.8 years) from Finland. As expected, age associated significantly with telomere length (p = .01). However, telomere length did not differ significantly between PD patients and controls (p = .54). Furthermore, extremely short telomeres were not more frequent in PD patients than in controls, as suggested in an earlier study. Our results do not support the concept of accelerated leukocyte telomere shortening in PD. |
| doi_str_mv | 10.1093/gerona/glq125 |
| format | Article |
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They become shorter after each cell division, and therefore, telomere length is considered as an indicator of cellular aging. Interestingly, both inflammation and oxidative stress, which play a role in the etiology of Parkinson’s disease (PD), may accelerate telomere shortening. Furthermore, it has been suggested that leukocyte telomere shortening may be accelerated in PD. To replicate the earlier findings, we analyzed telomere length of peripheral blood leukocytes in a sample of 131 PD patients (aged 66.8 ± 9.7 years) and 115 controls (aged 65.4 ± 9.8 years) from Finland. As expected, age associated significantly with telomere length (p = .01). However, telomere length did not differ significantly between PD patients and controls (p = .54). Furthermore, extremely short telomeres were not more frequent in PD patients than in controls, as suggested in an earlier study. Our results do not support the concept of accelerated leukocyte telomere shortening in PD.</description><identifier>ISSN: 1079-5006</identifier><identifier>EISSN: 1758-535X</identifier><identifier>DOI: 10.1093/gerona/glq125</identifier><identifier>PMID: 20639300</identifier><language>eng</language><publisher>United States: Oxford University Press</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Aging - physiology ; Case-Control Studies ; Cell division ; Chi-Square Distribution ; Chromosomes ; Female ; Gerontology ; Humans ; Leukocytes ; Leukocytes - ultrastructure ; Linear Models ; Male ; Middle Aged ; Oxidative stress ; Parkinson Disease - genetics ; Parkinson Disease - physiopathology ; Parkinson's disease ; Phenotype ; Telomere ; Telomere - ultrastructure</subject><ispartof>The journals of gerontology. Series A, Biological sciences and medical sciences, 2010-11, Vol.65A (11), p.1181-1184</ispartof><rights>The Author 2010. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org. 2010</rights><rights>Copyright Oxford University Press, UK Nov 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c429t-ef7e99fbc0481c6e675e31a108c8a3851fcdd00bc65f5667a239db9ce25c1d3a3</citedby><cites>FETCH-LOGICAL-c429t-ef7e99fbc0481c6e675e31a108c8a3851fcdd00bc65f5667a239db9ce25c1d3a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1578,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20639300$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Eerola, Johanna</creatorcontrib><creatorcontrib>Kananen, Laura</creatorcontrib><creatorcontrib>Manninen, Kaisa</creatorcontrib><creatorcontrib>Hellström, Olli</creatorcontrib><creatorcontrib>Tienari, Pentti J.</creatorcontrib><creatorcontrib>Hovatta, Iiris</creatorcontrib><title>No Evidence for Shorter Leukocyte Telomere Length in Parkinson’s Disease Patients</title><title>The journals of gerontology. Series A, Biological sciences and medical sciences</title><addtitle>J Gerontol A Biol Sci Med Sci</addtitle><description>Telomeres constitute the protective ends of chromosomes. They become shorter after each cell division, and therefore, telomere length is considered as an indicator of cellular aging. Interestingly, both inflammation and oxidative stress, which play a role in the etiology of Parkinson’s disease (PD), may accelerate telomere shortening. Furthermore, it has been suggested that leukocyte telomere shortening may be accelerated in PD. To replicate the earlier findings, we analyzed telomere length of peripheral blood leukocytes in a sample of 131 PD patients (aged 66.8 ± 9.7 years) and 115 controls (aged 65.4 ± 9.8 years) from Finland. As expected, age associated significantly with telomere length (p = .01). However, telomere length did not differ significantly between PD patients and controls (p = .54). Furthermore, extremely short telomeres were not more frequent in PD patients than in controls, as suggested in an earlier study. Our results do not support the concept of accelerated leukocyte telomere shortening in PD.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Aging - physiology</subject><subject>Case-Control Studies</subject><subject>Cell division</subject><subject>Chi-Square Distribution</subject><subject>Chromosomes</subject><subject>Female</subject><subject>Gerontology</subject><subject>Humans</subject><subject>Leukocytes</subject><subject>Leukocytes - ultrastructure</subject><subject>Linear Models</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Oxidative stress</subject><subject>Parkinson Disease - genetics</subject><subject>Parkinson Disease - physiopathology</subject><subject>Parkinson's disease</subject><subject>Phenotype</subject><subject>Telomere</subject><subject>Telomere - ultrastructure</subject><issn>1079-5006</issn><issn>1758-535X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkM9OGzEQh62qVUOBY6_Vqpf2suA_sb0-VgECUlQqBaSIi-V4Z8MmGzvYuxXceA1ejyfB0aY5cOlcZjT69JvRh9BXgk8IVux0AcE7c7poHgjlH9ABkbzIOeOzj2nGUuUcYzFAX2Jc4m1x-hkNKBZMMYwP0PS3z87_1iU4C1nlQza996GFkE2gW3n71EJ2A41fQ4C0cov2Pqtd9seEVe2id6_PLzE7qyOYCGnb1uDaeIQ-VaaJcLzrh-j24vxmdJlPrsdXo1-T3A6panOoJChVzS0eFsQKEJIDI4bgwhaGFZxUtiwxnlvBKy6ENJSpcq4sUG5JyQw7RD_63E3wDx3EVq_raKFpjAPfRZ1MFIxTQRP5_R259F1w6bkEKSwlpVso7yEbfIwBKr0J9dqEJ02w3rrWvWvdu078t11oN19Duaf_yU3Azx7w3ea_WbvbdWzhcQ8nzVpIJrm-nN1pMVZ0NhxP9Yi9AQnkmgE</recordid><startdate>201011</startdate><enddate>201011</enddate><creator>Eerola, Johanna</creator><creator>Kananen, Laura</creator><creator>Manninen, Kaisa</creator><creator>Hellström, Olli</creator><creator>Tienari, Pentti J.</creator><creator>Hovatta, Iiris</creator><general>Oxford University Press</general><scope>BSCLL</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>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>201011</creationdate><title>No Evidence for Shorter Leukocyte Telomere Length in Parkinson’s Disease Patients</title><author>Eerola, Johanna ; Kananen, Laura ; Manninen, Kaisa ; Hellström, Olli ; Tienari, Pentti J. ; Hovatta, Iiris</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c429t-ef7e99fbc0481c6e675e31a108c8a3851fcdd00bc65f5667a239db9ce25c1d3a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Aging - physiology</topic><topic>Case-Control Studies</topic><topic>Cell division</topic><topic>Chi-Square Distribution</topic><topic>Chromosomes</topic><topic>Female</topic><topic>Gerontology</topic><topic>Humans</topic><topic>Leukocytes</topic><topic>Leukocytes - ultrastructure</topic><topic>Linear Models</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Oxidative stress</topic><topic>Parkinson Disease - genetics</topic><topic>Parkinson Disease - physiopathology</topic><topic>Parkinson's disease</topic><topic>Phenotype</topic><topic>Telomere</topic><topic>Telomere - ultrastructure</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Eerola, Johanna</creatorcontrib><creatorcontrib>Kananen, Laura</creatorcontrib><creatorcontrib>Manninen, Kaisa</creatorcontrib><creatorcontrib>Hellström, Olli</creatorcontrib><creatorcontrib>Tienari, Pentti J.</creatorcontrib><creatorcontrib>Hovatta, Iiris</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>The journals of gerontology. 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They become shorter after each cell division, and therefore, telomere length is considered as an indicator of cellular aging. Interestingly, both inflammation and oxidative stress, which play a role in the etiology of Parkinson’s disease (PD), may accelerate telomere shortening. Furthermore, it has been suggested that leukocyte telomere shortening may be accelerated in PD. To replicate the earlier findings, we analyzed telomere length of peripheral blood leukocytes in a sample of 131 PD patients (aged 66.8 ± 9.7 years) and 115 controls (aged 65.4 ± 9.8 years) from Finland. As expected, age associated significantly with telomere length (p = .01). However, telomere length did not differ significantly between PD patients and controls (p = .54). Furthermore, extremely short telomeres were not more frequent in PD patients than in controls, as suggested in an earlier study. Our results do not support the concept of accelerated leukocyte telomere shortening in PD.</abstract><cop>United States</cop><pub>Oxford University Press</pub><pmid>20639300</pmid><doi>10.1093/gerona/glq125</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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| issn | 1079-5006 1758-535X |
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| source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; Alma/SFX Local Collection |
| subjects | Adult Aged Aged, 80 and over Aging - physiology Case-Control Studies Cell division Chi-Square Distribution Chromosomes Female Gerontology Humans Leukocytes Leukocytes - ultrastructure Linear Models Male Middle Aged Oxidative stress Parkinson Disease - genetics Parkinson Disease - physiopathology Parkinson's disease Phenotype Telomere Telomere - ultrastructure |
| title | No Evidence for Shorter Leukocyte Telomere Length in Parkinson’s Disease Patients |
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