A reciprocal relationship between markers of genomic DNA damage and alpha-synuclein pathology in dementia with Lewy bodies
DNA damage and DNA damage repair (DDR) dysfunction are insults with broad implications for cellular physiology and have been implicated in various neurodegenerative diseases. Alpha-synuclein (aSyn), a pre-synaptic and nuclear protein associated with neurodegenerative disorders known as synucleinopat...
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| Published in | Molecular neurodegeneration Vol. 20; no. 1; pp. 34 - 25 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
BioMed Central Ltd
20.03.2025
BMC |
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| Abstract | DNA damage and DNA damage repair (DDR) dysfunction are insults with broad implications for cellular physiology and have been implicated in various neurodegenerative diseases. Alpha-synuclein (aSyn), a pre-synaptic and nuclear protein associated with neurodegenerative disorders known as synucleinopathies, has been associated with DNA double strand break (DSB) repair. However, although nuclear aSyn pathology has been observed in cortical tissue of dementia with Lewy body (DLB) cases, whether such nuclear pathology coincides with the occurrence of DNA damage has not previously been investigated. Moreover, the specific types of DNA damage elevated in DLB cases and the contribution of DNA damage towards Lewy body (LB) formation is unknown.
DNA damage and aSyn pathology were assessed in fixed lateral temporal cortex from clinically and neuropathologically confirmed DLB cases and controls, as well as in cortical tissue from young 3-month-old presymptomatic A30P-aSyn mice. Frozen lateral temporal cortex from DLB and control cases was subject to nuclear isolation, western blotting, aSyn seed amplification and proteomic characterisation via mass spectrometry.
We detected seed-competent nuclear aSyn, and elevated nuclear serine-129 phosphorylation in DLB temporal cortex, alongside the accumulation of DSBs in neuronal and non-neuronal cellular populations. DNA damage was also present in cortical tissue from presymptomatic A30P mice, demonstrating it is an early insult closely associated with pathogenic aSyn. Strikingly, in postmortem DLB tissue, markers of genomic DNA damage-derived cytoplasmic DNA (CytoDNA) were evident within the majority of LBs examined. The observed cellular pathology was consistent with nuclear upregulation of associated DDR proteins, particularly those involved in base excision repair and DSB repair pathways.
Collectively our study demonstrates the accumulation of seed-competent pathological nuclear associated aSyn, alongside nuclear DNA damage and the potential involvement of DNA damage derived cytoDNA species in cytoplasmic aSyn pathology. Ultimately, our study supports the hypothesis of a reciprocal relationship between aSyn pathology and nuclear DNA damage and highlights a potential underlying role for DNA damage in pathological mechanisms relevant to DLB, as well as other synucleinopathies, opening novel possibilities for diagnosis and treatment. |
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| AbstractList | DNA damage and DNA damage repair (DDR) dysfunction are insults with broad implications for cellular physiology and have been implicated in various neurodegenerative diseases. Alpha-synuclein (aSyn), a pre-synaptic and nuclear protein associated with neurodegenerative disorders known as synucleinopathies, has been associated with DNA double strand break (DSB) repair. However, although nuclear aSyn pathology has been observed in cortical tissue of dementia with Lewy body (DLB) cases, whether such nuclear pathology coincides with the occurrence of DNA damage has not previously been investigated. Moreover, the specific types of DNA damage elevated in DLB cases and the contribution of DNA damage towards Lewy body (LB) formation is unknown.
DNA damage and aSyn pathology were assessed in fixed lateral temporal cortex from clinically and neuropathologically confirmed DLB cases and controls, as well as in cortical tissue from young 3-month-old presymptomatic A30P-aSyn mice. Frozen lateral temporal cortex from DLB and control cases was subject to nuclear isolation, western blotting, aSyn seed amplification and proteomic characterisation via mass spectrometry.
We detected seed-competent nuclear aSyn, and elevated nuclear serine-129 phosphorylation in DLB temporal cortex, alongside the accumulation of DSBs in neuronal and non-neuronal cellular populations. DNA damage was also present in cortical tissue from presymptomatic A30P mice, demonstrating it is an early insult closely associated with pathogenic aSyn. Strikingly, in postmortem DLB tissue, markers of genomic DNA damage-derived cytoplasmic DNA (CytoDNA) were evident within the majority of LBs examined. The observed cellular pathology was consistent with nuclear upregulation of associated DDR proteins, particularly those involved in base excision repair and DSB repair pathways.
Collectively our study demonstrates the accumulation of seed-competent pathological nuclear associated aSyn, alongside nuclear DNA damage and the potential involvement of DNA damage derived cytoDNA species in cytoplasmic aSyn pathology. Ultimately, our study supports the hypothesis of a reciprocal relationship between aSyn pathology and nuclear DNA damage and highlights a potential underlying role for DNA damage in pathological mechanisms relevant to DLB, as well as other synucleinopathies, opening novel possibilities for diagnosis and treatment. Abstract Background DNA damage and DNA damage repair (DDR) dysfunction are insults with broad implications for cellular physiology and have been implicated in various neurodegenerative diseases. Alpha-synuclein (aSyn), a pre-synaptic and nuclear protein associated with neurodegenerative disorders known as synucleinopathies, has been associated with DNA double strand break (DSB) repair. However, although nuclear aSyn pathology has been observed in cortical tissue of dementia with Lewy body (DLB) cases, whether such nuclear pathology coincides with the occurrence of DNA damage has not previously been investigated. Moreover, the specific types of DNA damage elevated in DLB cases and the contribution of DNA damage towards Lewy body (LB) formation is unknown. Methods DNA damage and aSyn pathology were assessed in fixed lateral temporal cortex from clinically and neuropathologically confirmed DLB cases and controls, as well as in cortical tissue from young 3-month-old presymptomatic A30P-aSyn mice. Frozen lateral temporal cortex from DLB and control cases was subject to nuclear isolation, western blotting, aSyn seed amplification and proteomic characterisation via mass spectrometry. Results We detected seed-competent nuclear aSyn, and elevated nuclear serine-129 phosphorylation in DLB temporal cortex, alongside the accumulation of DSBs in neuronal and non-neuronal cellular populations. DNA damage was also present in cortical tissue from presymptomatic A30P mice, demonstrating it is an early insult closely associated with pathogenic aSyn. Strikingly, in postmortem DLB tissue, markers of genomic DNA damage-derived cytoplasmic DNA (CytoDNA) were evident within the majority of LBs examined. The observed cellular pathology was consistent with nuclear upregulation of associated DDR proteins, particularly those involved in base excision repair and DSB repair pathways. Conclusions Collectively our study demonstrates the accumulation of seed-competent pathological nuclear associated aSyn, alongside nuclear DNA damage and the potential involvement of DNA damage derived cytoDNA species in cytoplasmic aSyn pathology. Ultimately, our study supports the hypothesis of a reciprocal relationship between aSyn pathology and nuclear DNA damage and highlights a potential underlying role for DNA damage in pathological mechanisms relevant to DLB, as well as other synucleinopathies, opening novel possibilities for diagnosis and treatment. DNA damage and DNA damage repair (DDR) dysfunction are insults with broad implications for cellular physiology and have been implicated in various neurodegenerative diseases. Alpha-synuclein (aSyn), a pre-synaptic and nuclear protein associated with neurodegenerative disorders known as synucleinopathies, has been associated with DNA double strand break (DSB) repair. However, although nuclear aSyn pathology has been observed in cortical tissue of dementia with Lewy body (DLB) cases, whether such nuclear pathology coincides with the occurrence of DNA damage has not previously been investigated. Moreover, the specific types of DNA damage elevated in DLB cases and the contribution of DNA damage towards Lewy body (LB) formation is unknown. DNA damage and aSyn pathology were assessed in fixed lateral temporal cortex from clinically and neuropathologically confirmed DLB cases and controls, as well as in cortical tissue from young 3-month-old presymptomatic A30P-aSyn mice. Frozen lateral temporal cortex from DLB and control cases was subject to nuclear isolation, western blotting, aSyn seed amplification and proteomic characterisation via mass spectrometry. We detected seed-competent nuclear aSyn, and elevated nuclear serine-129 phosphorylation in DLB temporal cortex, alongside the accumulation of DSBs in neuronal and non-neuronal cellular populations. DNA damage was also present in cortical tissue from presymptomatic A30P mice, demonstrating it is an early insult closely associated with pathogenic aSyn. Strikingly, in postmortem DLB tissue, markers of genomic DNA damage-derived cytoplasmic DNA (CytoDNA) were evident within the majority of LBs examined. The observed cellular pathology was consistent with nuclear upregulation of associated DDR proteins, particularly those involved in base excision repair and DSB repair pathways. Collectively our study demonstrates the accumulation of seed-competent pathological nuclear associated aSyn, alongside nuclear DNA damage and the potential involvement of DNA damage derived cytoDNA species in cytoplasmic aSyn pathology. Ultimately, our study supports the hypothesis of a reciprocal relationship between aSyn pathology and nuclear DNA damage and highlights a potential underlying role for DNA damage in pathological mechanisms relevant to DLB, as well as other synucleinopathies, opening novel possibilities for diagnosis and treatment. Background DNA damage and DNA damage repair (DDR) dysfunction are insults with broad implications for cellular physiology and have been implicated in various neurodegenerative diseases. Alpha-synuclein (aSyn), a pre-synaptic and nuclear protein associated with neurodegenerative disorders known as synucleinopathies, has been associated with DNA double strand break (DSB) repair. However, although nuclear aSyn pathology has been observed in cortical tissue of dementia with Lewy body (DLB) cases, whether such nuclear pathology coincides with the occurrence of DNA damage has not previously been investigated. Moreover, the specific types of DNA damage elevated in DLB cases and the contribution of DNA damage towards Lewy body (LB) formation is unknown. Methods DNA damage and aSyn pathology were assessed in fixed lateral temporal cortex from clinically and neuropathologically confirmed DLB cases and controls, as well as in cortical tissue from young 3-month-old presymptomatic A30P-aSyn mice. Frozen lateral temporal cortex from DLB and control cases was subject to nuclear isolation, western blotting, aSyn seed amplification and proteomic characterisation via mass spectrometry. Results We detected seed-competent nuclear aSyn, and elevated nuclear serine-129 phosphorylation in DLB temporal cortex, alongside the accumulation of DSBs in neuronal and non-neuronal cellular populations. DNA damage was also present in cortical tissue from presymptomatic A30P mice, demonstrating it is an early insult closely associated with pathogenic aSyn. Strikingly, in postmortem DLB tissue, markers of genomic DNA damage-derived cytoplasmic DNA (CytoDNA) were evident within the majority of LBs examined. The observed cellular pathology was consistent with nuclear upregulation of associated DDR proteins, particularly those involved in base excision repair and DSB repair pathways. Conclusions Collectively our study demonstrates the accumulation of seed-competent pathological nuclear associated aSyn, alongside nuclear DNA damage and the potential involvement of DNA damage derived cytoDNA species in cytoplasmic aSyn pathology. Ultimately, our study supports the hypothesis of a reciprocal relationship between aSyn pathology and nuclear DNA damage and highlights a potential underlying role for DNA damage in pathological mechanisms relevant to DLB, as well as other synucleinopathies, opening novel possibilities for diagnosis and treatment. Keywords: Dementia with Lewy bodies, Alpha-synuclein; DNA damage; synucleinopathy; Parkinson's disease DNA damage and DNA damage repair (DDR) dysfunction are insults with broad implications for cellular physiology and have been implicated in various neurodegenerative diseases. Alpha-synuclein (aSyn), a pre-synaptic and nuclear protein associated with neurodegenerative disorders known as synucleinopathies, has been associated with DNA double strand break (DSB) repair. However, although nuclear aSyn pathology has been observed in cortical tissue of dementia with Lewy body (DLB) cases, whether such nuclear pathology coincides with the occurrence of DNA damage has not previously been investigated. Moreover, the specific types of DNA damage elevated in DLB cases and the contribution of DNA damage towards Lewy body (LB) formation is unknown.BACKGROUNDDNA damage and DNA damage repair (DDR) dysfunction are insults with broad implications for cellular physiology and have been implicated in various neurodegenerative diseases. Alpha-synuclein (aSyn), a pre-synaptic and nuclear protein associated with neurodegenerative disorders known as synucleinopathies, has been associated with DNA double strand break (DSB) repair. However, although nuclear aSyn pathology has been observed in cortical tissue of dementia with Lewy body (DLB) cases, whether such nuclear pathology coincides with the occurrence of DNA damage has not previously been investigated. Moreover, the specific types of DNA damage elevated in DLB cases and the contribution of DNA damage towards Lewy body (LB) formation is unknown.DNA damage and aSyn pathology were assessed in fixed lateral temporal cortex from clinically and neuropathologically confirmed DLB cases and controls, as well as in cortical tissue from young 3-month-old presymptomatic A30P-aSyn mice. Frozen lateral temporal cortex from DLB and control cases was subject to nuclear isolation, western blotting, aSyn seed amplification and proteomic characterisation via mass spectrometry.METHODSDNA damage and aSyn pathology were assessed in fixed lateral temporal cortex from clinically and neuropathologically confirmed DLB cases and controls, as well as in cortical tissue from young 3-month-old presymptomatic A30P-aSyn mice. Frozen lateral temporal cortex from DLB and control cases was subject to nuclear isolation, western blotting, aSyn seed amplification and proteomic characterisation via mass spectrometry.We detected seed-competent nuclear aSyn, and elevated nuclear serine-129 phosphorylation in DLB temporal cortex, alongside the accumulation of DSBs in neuronal and non-neuronal cellular populations. DNA damage was also present in cortical tissue from presymptomatic A30P mice, demonstrating it is an early insult closely associated with pathogenic aSyn. Strikingly, in postmortem DLB tissue, markers of genomic DNA damage-derived cytoplasmic DNA (CytoDNA) were evident within the majority of LBs examined. The observed cellular pathology was consistent with nuclear upregulation of associated DDR proteins, particularly those involved in base excision repair and DSB repair pathways.RESULTSWe detected seed-competent nuclear aSyn, and elevated nuclear serine-129 phosphorylation in DLB temporal cortex, alongside the accumulation of DSBs in neuronal and non-neuronal cellular populations. DNA damage was also present in cortical tissue from presymptomatic A30P mice, demonstrating it is an early insult closely associated with pathogenic aSyn. Strikingly, in postmortem DLB tissue, markers of genomic DNA damage-derived cytoplasmic DNA (CytoDNA) were evident within the majority of LBs examined. The observed cellular pathology was consistent with nuclear upregulation of associated DDR proteins, particularly those involved in base excision repair and DSB repair pathways.Collectively our study demonstrates the accumulation of seed-competent pathological nuclear associated aSyn, alongside nuclear DNA damage and the potential involvement of DNA damage derived cytoDNA species in cytoplasmic aSyn pathology. Ultimately, our study supports the hypothesis of a reciprocal relationship between aSyn pathology and nuclear DNA damage and highlights a potential underlying role for DNA damage in pathological mechanisms relevant to DLB, as well as other synucleinopathies, opening novel possibilities for diagnosis and treatment.CONCLUSIONSCollectively our study demonstrates the accumulation of seed-competent pathological nuclear associated aSyn, alongside nuclear DNA damage and the potential involvement of DNA damage derived cytoDNA species in cytoplasmic aSyn pathology. Ultimately, our study supports the hypothesis of a reciprocal relationship between aSyn pathology and nuclear DNA damage and highlights a potential underlying role for DNA damage in pathological mechanisms relevant to DLB, as well as other synucleinopathies, opening novel possibilities for diagnosis and treatment. |
| ArticleNumber | 34 |
| Audience | Academic |
| Author | Anderson, Zoe Erskine, Daniel Morrice, Nicola Menon, Hariharan LeBeau, Fiona EN Attems, Johannes Yang, Tamsin Ghanem, Simona S. El-Agnaf, Omar Findlay, Lucas Koss, David J. Graham, Ben Walker, Lauren Todd, Olivia Palmowski, Pawel Porter, Andrew Outeiro, Tiago F. |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/40114198$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.3233/JAD-170342 10.1016/j.nbd.2020.105226 10.1158/0008-5472.CAN-11-2562 10.1038/s41598-019-47227-z 10.1093/nar/gku1003 10.1016/j.neuron.2018.07.039 10.1002/1531-8249(199912)46:6<920::AID-ANA17>3.0.CO;2-R 10.1212/WNL.58.12.1791 10.1269/jrr.08086 10.1038/s41586-020-2317-6 10.1093/mutage/geh025 10.1038/s12276-022-00727-x 10.1016/j.molcel.2020.12.021 10.1007/s00401-006-0081-9 10.1002/em.22087 10.1111/bpa.12344 10.1073/pnas.2109617119 10.1038/s41467-018-06331-w 10.1128/MCB.01053-08 10.1016/S0002-9440(10)65396-5 10.3390/cells11050906 10.1038/s41598-020-59364-x 10.1007/s00401-006-0127-z 10.1186/s13195-020-00727-x 10.1007/s00018-010-0408-5 10.1038/s42003-022-03312-0 10.1212/01.wnl.0000187889.17253.b1 10.1007/s00401-011-0910-3 10.1212/WNL.0000000000201199 10.1016/j.abb.2006.02.018 10.1186/s40478-018-0508-2 10.1016/j.neuron.2024.05.003 10.1093/hmg/ddx170 10.1016/j.nbd.2014.06.014 10.1016/j.jmb.2004.09.096 10.3390/biom11060820 10.1073/pnas.2118819119 10.1007/s00401-021-02329-9 10.1016/S0197-4580(02)00065-9 10.1007/s00401-020-02157-3 10.1073/pnas.1901313116 10.1038/nn.3537 10.1016/bs.pbr.2019.10.005 10.1093/hmg/ddac035 10.1093/nar/gkr463 10.1093/hmg/ddx114 10.1212/WNL.0000000000004058 10.3390/cancers13092235 10.1007/s12035-013-8406-x 10.1212/WNL.41.4.479 10.3390/cells10113239 10.1007/s00401-004-0937-9 10.1038/srep15299 10.1126/science.aao4426 10.1046/j.1471-4159.1997.69031196.x 10.1016/j.mrfmmm.2010.11.003 10.1016/S0027-5107(01)00091-4 10.1016/B978-0-12-803309-8.00017-3 10.1016/j.molcel.2005.10.003 10.3390/ijms23052484 10.1038/leu.2010.6 10.1016/j.bbrc.2016.11.008 10.1021/bi0341152 10.1371/journal.pone.0050245 10.1259/bjr.20130685 10.1186/s13024-016-0072-9 10.1093/nar/gkv1526 10.1016/j.jbc.2021.101552 10.1016/0896-6273(94)90264-X 10.1016/j.pneurobio.2022.102307 10.1074/jbc.273.42.27492 10.1093/hmg/ddy326 10.18632/oncotarget.8298 10.1523/JNEUROSCI.08-08-02804.1988 10.1186/s40478-022-01403-x 10.1016/j.nbd.2015.04.009 10.1016/j.neuroscience.2009.03.002 10.1371/journal.pone.0252635 10.1074/jbc.M303448200 10.1128/MCB.00488-18 10.1002/jcp.25048 10.7150/jca.23427 10.1093/nar/gkac1000 10.1007/s00702-005-0378-1 10.1523/JNEUROSCI.20-17-06365.2000 10.7554/eLife.62852 10.1038/s41467-021-23452-x 10.1016/j.parkreldis.2024.106077 10.3233/JAD-170397 10.1016/j.cell.2021.09.034 10.1016/j.neuron.2023.11.020 10.1111/j.0105-2896.2004.00162.x 10.1038/nprot.2008.211 10.3389/frdem.2024.1404841 10.1038/nmeth.3901 10.1128/MCB.00415-16 10.3389/fnins.2019.00381 10.3390/biom12050655 10.1093/jnen/62.6.644 10.1038/embor.2009.122 10.1093/nar/gkac194 10.1038/emm.2017.1 10.1186/s40478-019-0723-5 10.1007/s00702-017-1702-2 |
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| References | D Szklarczyk (813_CR46) 2015; 43 M Asada-Utsugi (813_CR78) 2022; 5 MS DeMott (813_CR99) 1998; 273 BT Sherman (813_CR47) 2022; 50 G Tetz (813_CR11) 2020; 10 H Braak (813_CR29) 2003; 24 ZM Kachaev (813_CR52) 2021; 10 ES Matsuo (813_CR77) 1994; 13 L Li (813_CR104) 2008; 28 NK Majbour (813_CR43) 2016; 11 IG McKeith (813_CR30) 2005; 65 LH Sanders (813_CR27) 2014; 70 MA Farg (813_CR14) 2017; 26 S Vispé (813_CR91) 2003; 278 J Goers (813_CR9) 2003; 42 J Fukae (813_CR89) 2005; 109 LJ Eccles (813_CR93) 2011; 711 813_CR19 W da Huang (813_CR48) 2009; 4 N Chatterjee (813_CR3) 2017; 58 L Maroteaux (813_CR62) 1988; 8 IG McKeith (813_CR31) 2017; 89 KN Miller (813_CR8) 2021; 184 A Kakarougkas (813_CR105) 2014; 87 BR Groveman (813_CR59) 2018; 6 JJ Morgan (813_CR54) 2021; 13 M Shaposhnikov (813_CR97) 2015; 5 813_CR41 D Cherny (813_CR10) 2004; 344 K Challa (813_CR55) 2021; 81 LJ Mah (813_CR63) 2010; 24 T Arai (813_CR87) 2006; 112 H Schell (813_CR38) 2012; 7 NR Belur (813_CR57) 2024; 112 SS Ghanem (813_CR72) 2022; 119 S Tyanova (813_CR45) 2016; 13 R De Bont (813_CR1) 2004; 19 Y Saito (813_CR80) 2003; 62 T Izumi (813_CR100) 2016 LA Parra-Rivas (813_CR76) 2023; 111 SK Singh (813_CR94) 2011; 39 WJ Cannan (813_CR66) 2016; 231 H Schell (813_CR68) 2009; 160 I Paiva (813_CR23) 2017; 26 NM Shanbhag (813_CR13) 2019; 7 JT Nimmo (813_CR75) 2020; 12 S Gonçalves (813_CR58) 2013; 47 KA Jellinger (813_CR70) 2018; 62 J Zhang (813_CR26) 1999; 154 BC Jung (813_CR61) 2017; 49 M Schweighauser (813_CR83) 2020; 585 DW Miller (813_CR71) 2005; 112 N Majbour (813_CR42) 2022; 99 A Van der Perren (813_CR84) 2020; 139 I Al-Musawi (813_CR39) 2024; 3 D Wang (813_CR16) 2016; 481 J Zhang (813_CR17) 2019; 13 MJ Keogh (813_CR6) 2018; 9 CC So (813_CR56) 2019; 39 ML Hegde (813_CR24) 2006; 449 C Morris (813_CR53) 2012; 72 B Sonustun (813_CR74) 2022; 11 MA Lodato (813_CR5) 2018; 359 AJ Espay (813_CR18) 2024; 122 S Wei (813_CR51) 2018; 9 PJ Kahle (813_CR36) 2000; 20 R Lopez-Gonzalez (813_CR98) 2019; 116 L Walker (813_CR40) 2017; 124 ZI Alam (813_CR25) 1997; 69 A Camins (813_CR65) 2010; 67 D Szklarczyk (813_CR49) 2023; 51 B Eftekharzadeh (813_CR79) 2018; 99 JT Hinkle (813_CR67) 2022; 119 L Li (813_CR103) 2016; 36 JH Power (813_CR85) 2017; 27 A Baude (813_CR102) 2015; 44 HM Geertsma (813_CR82) 2022; 31 TE Moors (813_CR73) 2021; 142 S Shadfar (813_CR7) 2022; 23 NN Vaikath (813_CR44) 2015; 79 813_CR81 TJ Montine (813_CR32) 2012; 123 PJ McKinnon (813_CR4) 2013; 16 AL Jackson (813_CR2) 2001; 477 N Zhang (813_CR101) 2009; 10 SS Mirra (813_CR35) 1991; 41 K Meek (813_CR96) 2004; 200 YS Yoon (813_CR22) 2022; 54 C Tweedy (813_CR37) 2021; 149 H Braak (813_CR34) 2006; 112 KM Miner (813_CR90) 2022; 216 DR Thal (813_CR33) 2002; 58 D Chowdhury (813_CR64) 2005; 20 I Poggiolini (813_CR60) 2021; 11 R Pinho (813_CR20) 2019; 28 DJ Koss (813_CR28) 2022; 10 SE Dent (813_CR50) 2022; 298 M Yousefzadeh (813_CR12) 2021; 10 H Matsui (813_CR86) 2021; 12 V Sharma (813_CR95) 2016; 7 C Chavarría (813_CR69) 2022; 12 V Vasquez (813_CR21) 2017; 60 N Shikazono (813_CR92) 2009; 50 AJ Schaser (813_CR15) 2019; 9 H Shimura-Miura (813_CR88) 1999; 46 |
| References_xml | – volume: 60 start-page: S133 issue: s1 year: 2017 ident: 813_CR21 publication-title: J Alzheimers Dis doi: 10.3233/JAD-170342 – volume: 149 start-page: 105226 year: 2021 ident: 813_CR37 publication-title: Neurobiol Dis doi: 10.1016/j.nbd.2020.105226 – volume: 72 start-page: 2006 issue: 8 year: 2012 ident: 813_CR53 publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-11-2562 – volume: 9 start-page: 10919 issue: 1 year: 2019 ident: 813_CR15 publication-title: Sci Rep doi: 10.1038/s41598-019-47227-z – volume: 43 start-page: D447 issue: Database issue year: 2015 ident: 813_CR46 publication-title: Nucleic Acids Res. doi: 10.1093/nar/gku1003 – volume: 99 start-page: 925 issue: 5 year: 2018 ident: 813_CR79 publication-title: Neuron doi: 10.1016/j.neuron.2018.07.039 – volume: 46 start-page: 920 issue: 6 year: 1999 ident: 813_CR88 publication-title: Ann Neurol doi: 10.1002/1531-8249(199912)46:6<920::AID-ANA17>3.0.CO;2-R – volume: 58 start-page: 1791 issue: 12 year: 2002 ident: 813_CR33 publication-title: Neurology doi: 10.1212/WNL.58.12.1791 – volume: 50 start-page: 27 issue: 1 year: 2009 ident: 813_CR92 publication-title: J Radiat Res doi: 10.1269/jrr.08086 – volume: 585 start-page: 464 issue: 7825 year: 2020 ident: 813_CR83 publication-title: Nature doi: 10.1038/s41586-020-2317-6 – volume: 19 start-page: 169 issue: 3 year: 2004 ident: 813_CR1 publication-title: Mutagenesis doi: 10.1093/mutage/geh025 – volume: 54 start-page: 115 issue: 2 year: 2022 ident: 813_CR22 publication-title: Exp Mol Med doi: 10.1038/s12276-022-00727-x – volume: 81 start-page: 811 issue: 4 year: 2021 ident: 813_CR55 publication-title: Mol Cell doi: 10.1016/j.molcel.2020.12.021 – volume: 112 start-page: 139 issue: 2 year: 2006 ident: 813_CR87 publication-title: Acta Neuropathol doi: 10.1007/s00401-006-0081-9 – volume: 58 start-page: 235 issue: 5 year: 2017 ident: 813_CR3 publication-title: Environ Mol Mutagen doi: 10.1002/em.22087 – volume: 27 start-page: 3 issue: 1 year: 2017 ident: 813_CR85 publication-title: Brain Pathol doi: 10.1111/bpa.12344 – volume: 119 start-page: e2109617119 issue: 15 year: 2022 ident: 813_CR72 publication-title: Proc Natl Acad Sci U S A doi: 10.1073/pnas.2109617119 – volume: 9 start-page: 4257 issue: 1 year: 2018 ident: 813_CR6 publication-title: Nat Commun doi: 10.1038/s41467-018-06331-w – volume: 28 start-page: 6413 issue: 20 year: 2008 ident: 813_CR104 publication-title: Mol Cell Biol doi: 10.1128/MCB.01053-08 – volume: 154 start-page: 1423 issue: 5 year: 1999 ident: 813_CR26 publication-title: Am J Pathol doi: 10.1016/S0002-9440(10)65396-5 – volume: 11 start-page: 906 issue: 5 year: 2022 ident: 813_CR74 publication-title: Cells. doi: 10.3390/cells11050906 – volume: 10 start-page: 2369 issue: 1 year: 2020 ident: 813_CR11 publication-title: Sci Rep doi: 10.1038/s41598-020-59364-x – volume: 112 start-page: 389 issue: 4 year: 2006 ident: 813_CR34 publication-title: Acta Neuropathol doi: 10.1007/s00401-006-0127-z – volume: 12 start-page: 159 issue: 1 year: 2020 ident: 813_CR75 publication-title: Alzheimers Res Ther doi: 10.1186/s13195-020-00727-x – volume: 67 start-page: 3865 issue: 22 year: 2010 ident: 813_CR65 publication-title: Cell Mol Life Sci doi: 10.1007/s00018-010-0408-5 – volume: 5 start-page: 358 issue: 1 year: 2022 ident: 813_CR78 publication-title: Commun Biol doi: 10.1038/s42003-022-03312-0 – volume: 65 start-page: 1863 issue: 12 year: 2005 ident: 813_CR30 publication-title: Neurology doi: 10.1212/01.wnl.0000187889.17253.b1 – volume: 123 start-page: 1 issue: 1 year: 2012 ident: 813_CR32 publication-title: Acta Neuropathol doi: 10.1007/s00401-011-0910-3 – volume: 99 start-page: e2417 issue: 21 year: 2022 ident: 813_CR42 publication-title: Neurology doi: 10.1212/WNL.0000000000201199 – volume: 449 start-page: 143 issue: 1–2 year: 2006 ident: 813_CR24 publication-title: Arch Biochem Biophys doi: 10.1016/j.abb.2006.02.018 – volume: 6 start-page: 7 issue: 1 year: 2018 ident: 813_CR59 publication-title: Acta Neuropathol Commun doi: 10.1186/s40478-018-0508-2 – volume: 112 start-page: 2558 issue: 15 year: 2024 ident: 813_CR57 publication-title: Neuron doi: 10.1016/j.neuron.2024.05.003 – volume: 26 start-page: 2882 issue: 15 year: 2017 ident: 813_CR14 publication-title: Hum Mol Genet doi: 10.1093/hmg/ddx170 – volume: 70 start-page: 214 year: 2014 ident: 813_CR27 publication-title: Neurobiol Dis doi: 10.1016/j.nbd.2014.06.014 – volume: 344 start-page: 929 issue: 4 year: 2004 ident: 813_CR10 publication-title: J Mol Biol doi: 10.1016/j.jmb.2004.09.096 – volume: 11 start-page: 820 issue: 6 year: 2021 ident: 813_CR60 publication-title: Biomolecules. doi: 10.3390/biom11060820 – volume: 119 start-page: e2118819119 issue: 15 year: 2022 ident: 813_CR67 publication-title: Proc Natl Acad Sci U S A doi: 10.1073/pnas.2118819119 – volume: 142 start-page: 423 issue: 3 year: 2021 ident: 813_CR73 publication-title: Acta Neuropathol doi: 10.1007/s00401-021-02329-9 – volume: 24 start-page: 197 issue: 2 year: 2003 ident: 813_CR29 publication-title: Neurobiol Aging doi: 10.1016/S0197-4580(02)00065-9 – volume: 139 start-page: 977 issue: 6 year: 2020 ident: 813_CR84 publication-title: Acta Neuropathol doi: 10.1007/s00401-020-02157-3 – volume: 116 start-page: 9628 issue: 19 year: 2019 ident: 813_CR98 publication-title: Proc Natl Acad Sci U S A doi: 10.1073/pnas.1901313116 – volume: 16 start-page: 1523 issue: 11 year: 2013 ident: 813_CR4 publication-title: Nat Neurosci doi: 10.1038/nn.3537 – ident: 813_CR19 doi: 10.1016/bs.pbr.2019.10.005 – volume: 31 start-page: 3613 issue: 21 year: 2022 ident: 813_CR82 publication-title: Hum Mol Genet doi: 10.1093/hmg/ddac035 – volume: 39 start-page: 8416 issue: 19 year: 2011 ident: 813_CR94 publication-title: Nucleic Acids Res doi: 10.1093/nar/gkr463 – volume: 26 start-page: 2231 issue: 12 year: 2017 ident: 813_CR23 publication-title: Hum Mol Genet doi: 10.1093/hmg/ddx114 – volume: 89 start-page: 88 issue: 1 year: 2017 ident: 813_CR31 publication-title: Neurology doi: 10.1212/WNL.0000000000004058 – volume: 13 start-page: 2235 issue: 9 year: 2021 ident: 813_CR54 publication-title: Cancers (Basel). doi: 10.3390/cancers13092235 – volume: 47 start-page: 1081 issue: 3 year: 2013 ident: 813_CR58 publication-title: Mol Neurobiol doi: 10.1007/s12035-013-8406-x – volume: 41 start-page: 479 issue: 4 year: 1991 ident: 813_CR35 publication-title: Neurology. doi: 10.1212/WNL.41.4.479 – volume: 10 start-page: 3239 issue: 11 year: 2021 ident: 813_CR52 publication-title: Cells doi: 10.3390/cells10113239 – volume: 109 start-page: 256 issue: 3 year: 2005 ident: 813_CR89 publication-title: Acta Neuropathologica. doi: 10.1007/s00401-004-0937-9 – volume: 5 start-page: 15299 issue: 1 year: 2015 ident: 813_CR97 publication-title: Sci Rep doi: 10.1038/srep15299 – volume: 359 start-page: 555 issue: 6375 year: 2018 ident: 813_CR5 publication-title: Science doi: 10.1126/science.aao4426 – volume: 69 start-page: 1196 issue: 3 year: 1997 ident: 813_CR25 publication-title: J Neurochem doi: 10.1046/j.1471-4159.1997.69031196.x – volume: 711 start-page: 134 issue: 1–2 year: 2011 ident: 813_CR93 publication-title: Mutat Res doi: 10.1016/j.mrfmmm.2010.11.003 – volume: 477 start-page: 7 issue: 1–2 year: 2001 ident: 813_CR2 publication-title: Mutat Res doi: 10.1016/S0027-5107(01)00091-4 – start-page: 275 volume-title: Genome Stability year: 2016 ident: 813_CR100 doi: 10.1016/B978-0-12-803309-8.00017-3 – volume: 20 start-page: 801 issue: 5 year: 2005 ident: 813_CR64 publication-title: Mol Cell doi: 10.1016/j.molcel.2005.10.003 – volume: 23 start-page: 2484 issue: 5 year: 2022 ident: 813_CR7 publication-title: Int J Mol Sci. doi: 10.3390/ijms23052484 – volume: 24 start-page: 679 issue: 4 year: 2010 ident: 813_CR63 publication-title: Leukemia doi: 10.1038/leu.2010.6 – volume: 481 start-page: 104 issue: 1–2 year: 2016 ident: 813_CR16 publication-title: Biochem Biophys Res Commun doi: 10.1016/j.bbrc.2016.11.008 – volume: 42 start-page: 8465 issue: 28 year: 2003 ident: 813_CR9 publication-title: Biochemistry doi: 10.1021/bi0341152 – volume: 7 start-page: e50245 issue: 11 year: 2012 ident: 813_CR38 publication-title: PLoS ONE doi: 10.1371/journal.pone.0050245 – volume: 87 start-page: 20130685 issue: 1035 year: 2014 ident: 813_CR105 publication-title: Br J Radiol doi: 10.1259/bjr.20130685 – volume: 11 start-page: 7 year: 2016 ident: 813_CR43 publication-title: Mol Neurodegener doi: 10.1186/s13024-016-0072-9 – volume: 44 start-page: 2214 issue: 5 year: 2015 ident: 813_CR102 publication-title: Nucleic Acids Res doi: 10.1093/nar/gkv1526 – volume: 298 start-page: 101552 issue: 2 year: 2022 ident: 813_CR50 publication-title: J Biol Chem doi: 10.1016/j.jbc.2021.101552 – volume: 13 start-page: 989 issue: 4 year: 1994 ident: 813_CR77 publication-title: Neuron doi: 10.1016/0896-6273(94)90264-X – volume: 216 start-page: 102307 year: 2022 ident: 813_CR90 publication-title: Prog Neurobiol doi: 10.1016/j.pneurobio.2022.102307 – volume: 273 start-page: 27492 issue: 42 year: 1998 ident: 813_CR99 publication-title: J Biol Chem doi: 10.1074/jbc.273.42.27492 – volume: 28 start-page: 31 issue: 1 year: 2019 ident: 813_CR20 publication-title: Hum Mol Genet doi: 10.1093/hmg/ddy326 – volume: 7 start-page: 25377 issue: 18 year: 2016 ident: 813_CR95 publication-title: Oncotarget doi: 10.18632/oncotarget.8298 – volume: 8 start-page: 2804 issue: 8 year: 1988 ident: 813_CR62 publication-title: J Neurosci doi: 10.1523/JNEUROSCI.08-08-02804.1988 – volume: 10 start-page: 98 issue: 1 year: 2022 ident: 813_CR28 publication-title: Acta Neuropathol Commun doi: 10.1186/s40478-022-01403-x – volume: 79 start-page: 81 year: 2015 ident: 813_CR44 publication-title: Neurobiol Dis doi: 10.1016/j.nbd.2015.04.009 – volume: 160 start-page: 796 issue: 4 year: 2009 ident: 813_CR68 publication-title: Neuroscience doi: 10.1016/j.neuroscience.2009.03.002 – ident: 813_CR81 doi: 10.1371/journal.pone.0252635 – ident: 813_CR41 – volume: 278 start-page: 35279 issue: 37 year: 2003 ident: 813_CR91 publication-title: J Biol Chem doi: 10.1074/jbc.M303448200 – volume: 39 start-page: e00488 issue: 8 year: 2019 ident: 813_CR56 publication-title: Mol Cell Biol. doi: 10.1128/MCB.00488-18 – volume: 231 start-page: 3 issue: 1 year: 2016 ident: 813_CR66 publication-title: J Cell Physiol doi: 10.1002/jcp.25048 – volume: 9 start-page: 2072 issue: 12 year: 2018 ident: 813_CR51 publication-title: J Cancer doi: 10.7150/jca.23427 – volume: 51 start-page: D638 issue: D1 year: 2023 ident: 813_CR49 publication-title: Nucleic Acids Res doi: 10.1093/nar/gkac1000 – volume: 112 start-page: 1613 issue: 12 year: 2005 ident: 813_CR71 publication-title: J Neural Transm (Vienna) doi: 10.1007/s00702-005-0378-1 – volume: 20 start-page: 6365 issue: 17 year: 2000 ident: 813_CR36 publication-title: J Neurosci doi: 10.1523/JNEUROSCI.20-17-06365.2000 – volume: 10 start-page: e62852 year: 2021 ident: 813_CR12 publication-title: Elife. doi: 10.7554/eLife.62852 – volume: 12 start-page: 3101 issue: 1 year: 2021 ident: 813_CR86 publication-title: Nat Commun doi: 10.1038/s41467-021-23452-x – volume: 122 start-page: 106077 year: 2024 ident: 813_CR18 publication-title: Parkinsonism Relat Disord doi: 10.1016/j.parkreldis.2024.106077 – volume: 62 start-page: 1141 issue: 3 year: 2018 ident: 813_CR70 publication-title: J Alzheimers Dis doi: 10.3233/JAD-170397 – volume: 184 start-page: 5506 issue: 22 year: 2021 ident: 813_CR8 publication-title: Cell doi: 10.1016/j.cell.2021.09.034 – volume: 111 start-page: 4006 issue: 24 year: 2023 ident: 813_CR76 publication-title: Neuron doi: 10.1016/j.neuron.2023.11.020 – volume: 200 start-page: 132 year: 2004 ident: 813_CR96 publication-title: Immunol Rev doi: 10.1111/j.0105-2896.2004.00162.x – volume: 4 start-page: 44 issue: 1 year: 2009 ident: 813_CR48 publication-title: Nat Protoc doi: 10.1038/nprot.2008.211 – volume: 3 start-page: 1404841 year: 2024 ident: 813_CR39 publication-title: Front Dementia. doi: 10.3389/frdem.2024.1404841 – volume: 13 start-page: 731 issue: 9 year: 2016 ident: 813_CR45 publication-title: Nat Methods doi: 10.1038/nmeth.3901 – volume: 36 start-page: 2794 issue: 22 year: 2016 ident: 813_CR103 publication-title: Mol Cell Biol doi: 10.1128/MCB.00415-16 – volume: 13 start-page: 381 year: 2019 ident: 813_CR17 publication-title: Front Neurosci. doi: 10.3389/fnins.2019.00381 – volume: 12 start-page: 655 issue: 5 year: 2022 ident: 813_CR69 publication-title: Biomolecules. doi: 10.3390/biom12050655 – volume: 62 start-page: 644 issue: 6 year: 2003 ident: 813_CR80 publication-title: J Neuropathol Exp Neurol doi: 10.1093/jnen/62.6.644 – volume: 10 start-page: 1029 issue: 9 year: 2009 ident: 813_CR101 publication-title: EMBO Rep doi: 10.1038/embor.2009.122 – volume: 50 start-page: W216 issue: W1 year: 2022 ident: 813_CR47 publication-title: Nucleic Acids Res doi: 10.1093/nar/gkac194 – volume: 49 start-page: e314 issue: 4 year: 2017 ident: 813_CR61 publication-title: Exp Mol Med doi: 10.1038/emm.2017.1 – volume: 7 start-page: 77 issue: 1 year: 2019 ident: 813_CR13 publication-title: Acta Neuropathol Commun doi: 10.1186/s40478-019-0723-5 – volume: 124 start-page: 671 issue: 6 year: 2017 ident: 813_CR40 publication-title: J Neural Transm (Vienna) doi: 10.1007/s00702-017-1702-2 |
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| Snippet | DNA damage and DNA damage repair (DDR) dysfunction are insults with broad implications for cellular physiology and have been implicated in various... Background DNA damage and DNA damage repair (DDR) dysfunction are insults with broad implications for cellular physiology and have been implicated in various... Abstract Background DNA damage and DNA damage repair (DDR) dysfunction are insults with broad implications for cellular physiology and have been implicated in... |
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| SubjectTerms | Aged Aged, 80 and over alpha-Synuclein - genetics alpha-Synuclein - metabolism Alpha-synuclein; DNA damage; synucleinopathy; Parkinson’s disease Animals Biomarkers - metabolism Brain Dementia with Lewy bodies DNA DNA damage DNA Damage - physiology Ethylenediaminetetraacetic acid Female Humans Lewy Bodies - metabolism Lewy Bodies - pathology Lewy Body Disease - genetics Lewy Body Disease - metabolism Lewy Body Disease - pathology Male Medical research Medicine, Experimental Mice Mice, Transgenic Nervous system diseases Neurons Neurophysiology Physiological aspects Proteins |
| Title | A reciprocal relationship between markers of genomic DNA damage and alpha-synuclein pathology in dementia with Lewy bodies |
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