Parkinson's disease and Alzheimer's disease: hypersensitivity to X rays in cultured cell lines
Fibroblast and/or lymphoblastoid lines from patients with several inherited primary neuronal degenerations are hypersensitive to DNA-damaging agents. Therefore, lymphoblastoid lines were irradiated from patients with sporadic Parkinson's disease (PD), Alzheimer's disease, and amyotrophic l...
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| Veröffentlicht in: | Journal of neurology, neurosurgery and psychiatry neurosurgery and psychiatry, 1985-09, Vol.48 (9), p.916-923 |
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| container_title | Journal of neurology, neurosurgery and psychiatry |
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| creator | Robbins, J H Otsuka, F Tarone, R E Polinsky, R J Brumback, R A Nee, L E |
| description | Fibroblast and/or lymphoblastoid lines from patients with several inherited primary neuronal degenerations are hypersensitive to DNA-damaging agents. Therefore, lymphoblastoid lines were irradiated from patients with sporadic Parkinson's disease (PD), Alzheimer's disease, and amyotrophic lateral sclerosis. The mean survival values of the eight Parkinson's disease and of the six Alzheimer's disease lines, but not of the five amyotrophic lateral sclerosis lines, were less than that of the 28 normal lines. Our results with Parkinson's disease and Alzheimer's disease cells can be explained by a genetic defect arising as a somatic mutation during embryogenesis, causing defective repair of the X-ray type of DNA damage. Such a DNA repair defect could cause an abnormal accumulation of spontaneously occurring DNA damage in Parkinson's disease and Alzheimer's disease neurons in vivo, resulting in their premature death. |
| doi_str_mv | 10.1136/jnnp.48.9.916 |
| format | Article |
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Therefore, lymphoblastoid lines were irradiated from patients with sporadic Parkinson's disease (PD), Alzheimer's disease, and amyotrophic lateral sclerosis. The mean survival values of the eight Parkinson's disease and of the six Alzheimer's disease lines, but not of the five amyotrophic lateral sclerosis lines, were less than that of the 28 normal lines. Our results with Parkinson's disease and Alzheimer's disease cells can be explained by a genetic defect arising as a somatic mutation during embryogenesis, causing defective repair of the X-ray type of DNA damage. Such a DNA repair defect could cause an abnormal accumulation of spontaneously occurring DNA damage in Parkinson's disease and Alzheimer's disease neurons in vivo, resulting in their premature death.</description><identifier>ISSN: 0022-3050</identifier><identifier>EISSN: 1468-330X</identifier><identifier>DOI: 10.1136/jnnp.48.9.916</identifier><identifier>PMID: 3876409</identifier><identifier>CODEN: JNNPAU</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd</publisher><subject>Adolescent ; Adult ; Aged ; Alzheimer Disease - etiology ; Alzheimer Disease - physiopathology ; Amyotrophic Lateral Sclerosis - physiopathology ; B-Lymphocytes - radiation effects ; Biological and medical sciences ; Cell Line ; Child ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; DNA - radiation effects ; Female ; Humans ; Male ; Medical sciences ; Middle Aged ; Neurology ; Parkinson Disease - etiology ; Parkinson Disease - physiopathology ; Radiation Tolerance ; Ultraviolet Rays - adverse effects ; Xeroderma Pigmentosum - physiopathology</subject><ispartof>Journal of neurology, neurosurgery and psychiatry, 1985-09, Vol.48 (9), p.916-923</ispartof><rights>1986 INIST-CNRS</rights><rights>Copyright BMJ Publishing Group LTD Sep 1985</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b510t-5b9947aaf0ac063f51bd5990b91557b953bac6996620df51d1b501bbe5f686573</citedby><cites>FETCH-LOGICAL-b510t-5b9947aaf0ac063f51bd5990b91557b953bac6996620df51d1b501bbe5f686573</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1028494/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1028494/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,724,777,781,882,27905,27906,53772,53774</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=8503612$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/3876409$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Robbins, J H</creatorcontrib><creatorcontrib>Otsuka, F</creatorcontrib><creatorcontrib>Tarone, R E</creatorcontrib><creatorcontrib>Polinsky, R J</creatorcontrib><creatorcontrib>Brumback, R A</creatorcontrib><creatorcontrib>Nee, L E</creatorcontrib><title>Parkinson's disease and Alzheimer's disease: hypersensitivity to X rays in cultured cell lines</title><title>Journal of neurology, neurosurgery and psychiatry</title><addtitle>J Neurol Neurosurg Psychiatry</addtitle><description>Fibroblast and/or lymphoblastoid lines from patients with several inherited primary neuronal degenerations are hypersensitive to DNA-damaging agents. Therefore, lymphoblastoid lines were irradiated from patients with sporadic Parkinson's disease (PD), Alzheimer's disease, and amyotrophic lateral sclerosis. The mean survival values of the eight Parkinson's disease and of the six Alzheimer's disease lines, but not of the five amyotrophic lateral sclerosis lines, were less than that of the 28 normal lines. Our results with Parkinson's disease and Alzheimer's disease cells can be explained by a genetic defect arising as a somatic mutation during embryogenesis, causing defective repair of the X-ray type of DNA damage. Such a DNA repair defect could cause an abnormal accumulation of spontaneously occurring DNA damage in Parkinson's disease and Alzheimer's disease neurons in vivo, resulting in their premature death.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Alzheimer Disease - etiology</subject><subject>Alzheimer Disease - physiopathology</subject><subject>Amyotrophic Lateral Sclerosis - physiopathology</subject><subject>B-Lymphocytes - radiation effects</subject><subject>Biological and medical sciences</subject><subject>Cell Line</subject><subject>Child</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>DNA - radiation effects</subject><subject>Female</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Neurology</subject><subject>Parkinson Disease - etiology</subject><subject>Parkinson Disease - physiopathology</subject><subject>Radiation Tolerance</subject><subject>Ultraviolet Rays - adverse effects</subject><subject>Xeroderma Pigmentosum - physiopathology</subject><issn>0022-3050</issn><issn>1468-330X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1985</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkd1rFDEUxYModVt99FEIKNWXWZPJ5MsHoSzWCkXFL_pkSGYybrYzmTV3prj-9WbZZau-mJcLOT_OPZeD0CNK5pQy8WIV43peqbmeayruoBmthCoYI1d30YyQsiwY4eQ-OgZYke1T-ggdMSVFRfQMfftg03WIMMRngJsA3oLHNjb4rPu19KH36fb_JV5u1j6BjxDGcBPGDR4HfIWT3QAOEddTN07JN7j2XYe7ED08QPda24F_uJ8n6Mv568-Li-Ly_Zu3i7PLwnFKxoI7rStpbUtsTQRrOXUN15o4TTmXTnPmbC20FqIkTVYb6jihznneCiW4ZCfo1c53PbneN7WPY7KdWafQ27Qxgw3mbyWGpfk-3BhKSlXpKhuc7g3S8GPyMJo-wPYOG_0wgZGCabIDn_wDroYpxXycoVKWStKqZJkqdlSdBoDk20MUSsy2NrOtzVTKaJNry_zjP_Mf6H1PWX-61y3UtmuTjXWAA6Y4YYKWt2sDjP7nQc4VGyGZ5Obd14X5WJ4r9YmX5iLzz3e861f_SfgbwE29eg</recordid><startdate>19850901</startdate><enddate>19850901</enddate><creator>Robbins, J H</creator><creator>Otsuka, F</creator><creator>Tarone, R E</creator><creator>Polinsky, R J</creator><creator>Brumback, R A</creator><creator>Nee, L E</creator><general>BMJ Publishing Group Ltd</general><general>BMJ</general><general>BMJ Publishing Group LTD</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>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>8AF</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M2P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19850901</creationdate><title>Parkinson's disease and Alzheimer's disease: hypersensitivity to X rays in cultured cell lines</title><author>Robbins, J H ; Otsuka, F ; Tarone, R E ; Polinsky, R J ; Brumback, R A ; Nee, L E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b510t-5b9947aaf0ac063f51bd5990b91557b953bac6996620df51d1b501bbe5f686573</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1985</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Alzheimer Disease - etiology</topic><topic>Alzheimer Disease - physiopathology</topic><topic>Amyotrophic Lateral Sclerosis - physiopathology</topic><topic>B-Lymphocytes - radiation effects</topic><topic>Biological and medical sciences</topic><topic>Cell Line</topic><topic>Child</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>DNA - radiation effects</topic><topic>Female</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Neurology</topic><topic>Parkinson Disease - etiology</topic><topic>Parkinson Disease - physiopathology</topic><topic>Radiation Tolerance</topic><topic>Ultraviolet Rays - adverse effects</topic><topic>Xeroderma Pigmentosum - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Robbins, J H</creatorcontrib><creatorcontrib>Otsuka, F</creatorcontrib><creatorcontrib>Tarone, R E</creatorcontrib><creatorcontrib>Polinsky, R J</creatorcontrib><creatorcontrib>Brumback, R A</creatorcontrib><creatorcontrib>Nee, L E</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</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 Central (Corporate)</collection><collection>ProQuest Nursing and Allied Health Journals</collection><collection>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Psychology Journals</collection><collection>ProQuest Science Journals</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of neurology, neurosurgery and psychiatry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Robbins, J H</au><au>Otsuka, F</au><au>Tarone, R E</au><au>Polinsky, R J</au><au>Brumback, R A</au><au>Nee, L E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Parkinson's disease and Alzheimer's disease: hypersensitivity to X rays in cultured cell lines</atitle><jtitle>Journal of neurology, neurosurgery and psychiatry</jtitle><addtitle>J Neurol Neurosurg Psychiatry</addtitle><date>1985-09-01</date><risdate>1985</risdate><volume>48</volume><issue>9</issue><spage>916</spage><epage>923</epage><pages>916-923</pages><issn>0022-3050</issn><eissn>1468-330X</eissn><coden>JNNPAU</coden><abstract>Fibroblast and/or lymphoblastoid lines from patients with several inherited primary neuronal degenerations are hypersensitive to DNA-damaging agents. Therefore, lymphoblastoid lines were irradiated from patients with sporadic Parkinson's disease (PD), Alzheimer's disease, and amyotrophic lateral sclerosis. The mean survival values of the eight Parkinson's disease and of the six Alzheimer's disease lines, but not of the five amyotrophic lateral sclerosis lines, were less than that of the 28 normal lines. Our results with Parkinson's disease and Alzheimer's disease cells can be explained by a genetic defect arising as a somatic mutation during embryogenesis, causing defective repair of the X-ray type of DNA damage. Such a DNA repair defect could cause an abnormal accumulation of spontaneously occurring DNA damage in Parkinson's disease and Alzheimer's disease neurons in vivo, resulting in their premature death.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd</pub><pmid>3876409</pmid><doi>10.1136/jnnp.48.9.916</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 0022-3050 |
| ispartof | Journal of neurology, neurosurgery and psychiatry, 1985-09, Vol.48 (9), p.916-923 |
| issn | 0022-3050 1468-330X |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_1028494 |
| source | MEDLINE; PubMed Central; Alma/SFX Local Collection; EZB Electronic Journals Library |
| subjects | Adolescent Adult Aged Alzheimer Disease - etiology Alzheimer Disease - physiopathology Amyotrophic Lateral Sclerosis - physiopathology B-Lymphocytes - radiation effects Biological and medical sciences Cell Line Child Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases DNA - radiation effects Female Humans Male Medical sciences Middle Aged Neurology Parkinson Disease - etiology Parkinson Disease - physiopathology Radiation Tolerance Ultraviolet Rays - adverse effects Xeroderma Pigmentosum - physiopathology |
| title | Parkinson's disease and Alzheimer's disease: hypersensitivity to X rays in cultured cell lines |
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