Parkinson’s disease and Alzheimer’s disease: a Mendelian randomization study

Abstract Background Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the top two common neurodegenerative diseases in elderly. Recent studies found the α-synuclein have a key role in AD. Although many clinical and pathological features between AD and PD are shared, the genetic association b...
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Autor*in:	Zhifa Han [verfasserIn] Rui Tian [verfasserIn] Peng Ren [verfasserIn] Wenyang Zhou [verfasserIn] Pingping Wang [verfasserIn] Meng Luo [verfasserIn] Shuilin Jin [verfasserIn] Qinghua Jiang [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2018

Schlagwörter:	Alzheimer’s disease Parkinson’s disease α-synuclein Mendelian randomization Genetic association

Übergeordnetes Werk:	In: BMC Medical Genetics - BMC, 2003, 19(2018), S1, Seite 9
Übergeordnetes Werk:	volume:19 ; year:2018 ; number:S1 ; pages:9

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/s12881-018-0721-7

Katalog-ID:	DOAJ057035458

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520			\|a Abstract Background Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the top two common neurodegenerative diseases in elderly. Recent studies found the α-synuclein have a key role in AD. Although many clinical and pathological features between AD and PD are shared, the genetic association between them remains unclear, especially whether α-synuclein in PD genetically alters AD risk. Results We did not obtain any significant result (OR = 0.918, 95% CI: 0.782–1.076, P = 0.291) in MR analysis between PD and AD risk. In MR between α-synuclein in PD with AD risk, we only extracted rs356182 as the IV through a strict screening process. The result indicated a significant association based on IVW method (OR = 0.638, 95% CI: 0.485–0.838, P = 1.20E-03). In order to examine the robustness of the IVW method, we used other three complementary analytical methods and also obtained consistent results. Conclusion The overall PD genetic risk factors did not predict AD risk, but the α-synuclein susceptibility genetic variants in PD reduce the AD risk. We believe that our findings may help to understand the association between them, which may be useful for future genetic studies for both diseases.
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allfields	10.1186/s12881-018-0721-7 doi (DE-627)DOAJ057035458 (DE-599)DOAJ3b3d5a6b4dc2498391da937cf0c57043 DE-627 ger DE-627 rakwb eng RC31-1245 QH426-470 Zhifa Han verfasserin aut Parkinson’s disease and Alzheimer’s disease: a Mendelian randomization study 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the top two common neurodegenerative diseases in elderly. Recent studies found the α-synuclein have a key role in AD. Although many clinical and pathological features between AD and PD are shared, the genetic association between them remains unclear, especially whether α-synuclein in PD genetically alters AD risk. Results We did not obtain any significant result (OR = 0.918, 95% CI: 0.782–1.076, P = 0.291) in MR analysis between PD and AD risk. In MR between α-synuclein in PD with AD risk, we only extracted rs356182 as the IV through a strict screening process. The result indicated a significant association based on IVW method (OR = 0.638, 95% CI: 0.485–0.838, P = 1.20E-03). In order to examine the robustness of the IVW method, we used other three complementary analytical methods and also obtained consistent results. Conclusion The overall PD genetic risk factors did not predict AD risk, but the α-synuclein susceptibility genetic variants in PD reduce the AD risk. We believe that our findings may help to understand the association between them, which may be useful for future genetic studies for both diseases. Alzheimer’s disease Parkinson’s disease α-synuclein Mendelian randomization Genetic association Internal medicine Genetics Rui Tian verfasserin aut Peng Ren verfasserin aut Wenyang Zhou verfasserin aut Pingping Wang verfasserin aut Meng Luo verfasserin aut Shuilin Jin verfasserin aut Qinghua Jiang verfasserin aut In BMC Medical Genetics BMC, 2003 19(2018), S1, Seite 9 (DE-627)326643788 (DE-600)2041359-2 14712350 nnns volume:19 year:2018 number:S1 pages:9 https://doi.org/10.1186/s12881-018-0721-7 kostenfrei https://doaj.org/article/3b3d5a6b4dc2498391da937cf0c57043 kostenfrei http://link.springer.com/article/10.1186/s12881-018-0721-7 kostenfrei https://doaj.org/toc/1471-2350 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 19 2018 S1 9
spelling	10.1186/s12881-018-0721-7 doi (DE-627)DOAJ057035458 (DE-599)DOAJ3b3d5a6b4dc2498391da937cf0c57043 DE-627 ger DE-627 rakwb eng RC31-1245 QH426-470 Zhifa Han verfasserin aut Parkinson’s disease and Alzheimer’s disease: a Mendelian randomization study 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the top two common neurodegenerative diseases in elderly. Recent studies found the α-synuclein have a key role in AD. Although many clinical and pathological features between AD and PD are shared, the genetic association between them remains unclear, especially whether α-synuclein in PD genetically alters AD risk. Results We did not obtain any significant result (OR = 0.918, 95% CI: 0.782–1.076, P = 0.291) in MR analysis between PD and AD risk. In MR between α-synuclein in PD with AD risk, we only extracted rs356182 as the IV through a strict screening process. The result indicated a significant association based on IVW method (OR = 0.638, 95% CI: 0.485–0.838, P = 1.20E-03). In order to examine the robustness of the IVW method, we used other three complementary analytical methods and also obtained consistent results. Conclusion The overall PD genetic risk factors did not predict AD risk, but the α-synuclein susceptibility genetic variants in PD reduce the AD risk. We believe that our findings may help to understand the association between them, which may be useful for future genetic studies for both diseases. Alzheimer’s disease Parkinson’s disease α-synuclein Mendelian randomization Genetic association Internal medicine Genetics Rui Tian verfasserin aut Peng Ren verfasserin aut Wenyang Zhou verfasserin aut Pingping Wang verfasserin aut Meng Luo verfasserin aut Shuilin Jin verfasserin aut Qinghua Jiang verfasserin aut In BMC Medical Genetics BMC, 2003 19(2018), S1, Seite 9 (DE-627)326643788 (DE-600)2041359-2 14712350 nnns volume:19 year:2018 number:S1 pages:9 https://doi.org/10.1186/s12881-018-0721-7 kostenfrei https://doaj.org/article/3b3d5a6b4dc2498391da937cf0c57043 kostenfrei http://link.springer.com/article/10.1186/s12881-018-0721-7 kostenfrei https://doaj.org/toc/1471-2350 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 19 2018 S1 9
allfields_unstemmed	10.1186/s12881-018-0721-7 doi (DE-627)DOAJ057035458 (DE-599)DOAJ3b3d5a6b4dc2498391da937cf0c57043 DE-627 ger DE-627 rakwb eng RC31-1245 QH426-470 Zhifa Han verfasserin aut Parkinson’s disease and Alzheimer’s disease: a Mendelian randomization study 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the top two common neurodegenerative diseases in elderly. Recent studies found the α-synuclein have a key role in AD. Although many clinical and pathological features between AD and PD are shared, the genetic association between them remains unclear, especially whether α-synuclein in PD genetically alters AD risk. Results We did not obtain any significant result (OR = 0.918, 95% CI: 0.782–1.076, P = 0.291) in MR analysis between PD and AD risk. In MR between α-synuclein in PD with AD risk, we only extracted rs356182 as the IV through a strict screening process. The result indicated a significant association based on IVW method (OR = 0.638, 95% CI: 0.485–0.838, P = 1.20E-03). In order to examine the robustness of the IVW method, we used other three complementary analytical methods and also obtained consistent results. Conclusion The overall PD genetic risk factors did not predict AD risk, but the α-synuclein susceptibility genetic variants in PD reduce the AD risk. We believe that our findings may help to understand the association between them, which may be useful for future genetic studies for both diseases. Alzheimer’s disease Parkinson’s disease α-synuclein Mendelian randomization Genetic association Internal medicine Genetics Rui Tian verfasserin aut Peng Ren verfasserin aut Wenyang Zhou verfasserin aut Pingping Wang verfasserin aut Meng Luo verfasserin aut Shuilin Jin verfasserin aut Qinghua Jiang verfasserin aut In BMC Medical Genetics BMC, 2003 19(2018), S1, Seite 9 (DE-627)326643788 (DE-600)2041359-2 14712350 nnns volume:19 year:2018 number:S1 pages:9 https://doi.org/10.1186/s12881-018-0721-7 kostenfrei https://doaj.org/article/3b3d5a6b4dc2498391da937cf0c57043 kostenfrei http://link.springer.com/article/10.1186/s12881-018-0721-7 kostenfrei https://doaj.org/toc/1471-2350 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 19 2018 S1 9
allfieldsGer	10.1186/s12881-018-0721-7 doi (DE-627)DOAJ057035458 (DE-599)DOAJ3b3d5a6b4dc2498391da937cf0c57043 DE-627 ger DE-627 rakwb eng RC31-1245 QH426-470 Zhifa Han verfasserin aut Parkinson’s disease and Alzheimer’s disease: a Mendelian randomization study 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the top two common neurodegenerative diseases in elderly. Recent studies found the α-synuclein have a key role in AD. Although many clinical and pathological features between AD and PD are shared, the genetic association between them remains unclear, especially whether α-synuclein in PD genetically alters AD risk. Results We did not obtain any significant result (OR = 0.918, 95% CI: 0.782–1.076, P = 0.291) in MR analysis between PD and AD risk. In MR between α-synuclein in PD with AD risk, we only extracted rs356182 as the IV through a strict screening process. The result indicated a significant association based on IVW method (OR = 0.638, 95% CI: 0.485–0.838, P = 1.20E-03). In order to examine the robustness of the IVW method, we used other three complementary analytical methods and also obtained consistent results. Conclusion The overall PD genetic risk factors did not predict AD risk, but the α-synuclein susceptibility genetic variants in PD reduce the AD risk. We believe that our findings may help to understand the association between them, which may be useful for future genetic studies for both diseases. Alzheimer’s disease Parkinson’s disease α-synuclein Mendelian randomization Genetic association Internal medicine Genetics Rui Tian verfasserin aut Peng Ren verfasserin aut Wenyang Zhou verfasserin aut Pingping Wang verfasserin aut Meng Luo verfasserin aut Shuilin Jin verfasserin aut Qinghua Jiang verfasserin aut In BMC Medical Genetics BMC, 2003 19(2018), S1, Seite 9 (DE-627)326643788 (DE-600)2041359-2 14712350 nnns volume:19 year:2018 number:S1 pages:9 https://doi.org/10.1186/s12881-018-0721-7 kostenfrei https://doaj.org/article/3b3d5a6b4dc2498391da937cf0c57043 kostenfrei http://link.springer.com/article/10.1186/s12881-018-0721-7 kostenfrei https://doaj.org/toc/1471-2350 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 19 2018 S1 9
allfieldsSound	10.1186/s12881-018-0721-7 doi (DE-627)DOAJ057035458 (DE-599)DOAJ3b3d5a6b4dc2498391da937cf0c57043 DE-627 ger DE-627 rakwb eng RC31-1245 QH426-470 Zhifa Han verfasserin aut Parkinson’s disease and Alzheimer’s disease: a Mendelian randomization study 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the top two common neurodegenerative diseases in elderly. Recent studies found the α-synuclein have a key role in AD. Although many clinical and pathological features between AD and PD are shared, the genetic association between them remains unclear, especially whether α-synuclein in PD genetically alters AD risk. Results We did not obtain any significant result (OR = 0.918, 95% CI: 0.782–1.076, P = 0.291) in MR analysis between PD and AD risk. In MR between α-synuclein in PD with AD risk, we only extracted rs356182 as the IV through a strict screening process. The result indicated a significant association based on IVW method (OR = 0.638, 95% CI: 0.485–0.838, P = 1.20E-03). In order to examine the robustness of the IVW method, we used other three complementary analytical methods and also obtained consistent results. Conclusion The overall PD genetic risk factors did not predict AD risk, but the α-synuclein susceptibility genetic variants in PD reduce the AD risk. We believe that our findings may help to understand the association between them, which may be useful for future genetic studies for both diseases. Alzheimer’s disease Parkinson’s disease α-synuclein Mendelian randomization Genetic association Internal medicine Genetics Rui Tian verfasserin aut Peng Ren verfasserin aut Wenyang Zhou verfasserin aut Pingping Wang verfasserin aut Meng Luo verfasserin aut Shuilin Jin verfasserin aut Qinghua Jiang verfasserin aut In BMC Medical Genetics BMC, 2003 19(2018), S1, Seite 9 (DE-627)326643788 (DE-600)2041359-2 14712350 nnns volume:19 year:2018 number:S1 pages:9 https://doi.org/10.1186/s12881-018-0721-7 kostenfrei https://doaj.org/article/3b3d5a6b4dc2498391da937cf0c57043 kostenfrei http://link.springer.com/article/10.1186/s12881-018-0721-7 kostenfrei https://doaj.org/toc/1471-2350 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 19 2018 S1 9
language	English
source	In BMC Medical Genetics 19(2018), S1, Seite 9 volume:19 year:2018 number:S1 pages:9
sourceStr	In BMC Medical Genetics 19(2018), S1, Seite 9 volume:19 year:2018 number:S1 pages:9
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Alzheimer’s disease Parkinson’s disease α-synuclein Mendelian randomization Genetic association Internal medicine Genetics
isfreeaccess_bool	true
container_title	BMC Medical Genetics
authorswithroles_txt_mv	Zhifa Han @@aut@@ Rui Tian @@aut@@ Peng Ren @@aut@@ Wenyang Zhou @@aut@@ Pingping Wang @@aut@@ Meng Luo @@aut@@ Shuilin Jin @@aut@@ Qinghua Jiang @@aut@@
publishDateDaySort_date	2018-01-01T00:00:00Z
hierarchy_top_id	326643788
id	DOAJ057035458
language_de	englisch
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callnumber-first	R - Medicine
author	Zhifa Han
spellingShingle	Zhifa Han misc RC31-1245 misc QH426-470 misc Alzheimer’s disease misc Parkinson’s disease misc α-synuclein misc Mendelian randomization misc Genetic association misc Internal medicine misc Genetics Parkinson’s disease and Alzheimer’s disease: a Mendelian randomization study
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topic_title	RC31-1245 QH426-470 Parkinson’s disease and Alzheimer’s disease: a Mendelian randomization study Alzheimer’s disease Parkinson’s disease α-synuclein Mendelian randomization Genetic association
topic	misc RC31-1245 misc QH426-470 misc Alzheimer’s disease misc Parkinson’s disease misc α-synuclein misc Mendelian randomization misc Genetic association misc Internal medicine misc Genetics
topic_unstemmed	misc RC31-1245 misc QH426-470 misc Alzheimer’s disease misc Parkinson’s disease misc α-synuclein misc Mendelian randomization misc Genetic association misc Internal medicine misc Genetics
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title	Parkinson’s disease and Alzheimer’s disease: a Mendelian randomization study
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title_full	Parkinson’s disease and Alzheimer’s disease: a Mendelian randomization study
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journal	BMC Medical Genetics
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author_browse	Zhifa Han Rui Tian Peng Ren Wenyang Zhou Pingping Wang Meng Luo Shuilin Jin Qinghua Jiang
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title_sort	parkinson’s disease and alzheimer’s disease: a mendelian randomization study
callnumber	RC31-1245
title_auth	Parkinson’s disease and Alzheimer’s disease: a Mendelian randomization study
abstract	Abstract Background Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the top two common neurodegenerative diseases in elderly. Recent studies found the α-synuclein have a key role in AD. Although many clinical and pathological features between AD and PD are shared, the genetic association between them remains unclear, especially whether α-synuclein in PD genetically alters AD risk. Results We did not obtain any significant result (OR = 0.918, 95% CI: 0.782–1.076, P = 0.291) in MR analysis between PD and AD risk. In MR between α-synuclein in PD with AD risk, we only extracted rs356182 as the IV through a strict screening process. The result indicated a significant association based on IVW method (OR = 0.638, 95% CI: 0.485–0.838, P = 1.20E-03). In order to examine the robustness of the IVW method, we used other three complementary analytical methods and also obtained consistent results. Conclusion The overall PD genetic risk factors did not predict AD risk, but the α-synuclein susceptibility genetic variants in PD reduce the AD risk. We believe that our findings may help to understand the association between them, which may be useful for future genetic studies for both diseases.
abstractGer	Abstract Background Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the top two common neurodegenerative diseases in elderly. Recent studies found the α-synuclein have a key role in AD. Although many clinical and pathological features between AD and PD are shared, the genetic association between them remains unclear, especially whether α-synuclein in PD genetically alters AD risk. Results We did not obtain any significant result (OR = 0.918, 95% CI: 0.782–1.076, P = 0.291) in MR analysis between PD and AD risk. In MR between α-synuclein in PD with AD risk, we only extracted rs356182 as the IV through a strict screening process. The result indicated a significant association based on IVW method (OR = 0.638, 95% CI: 0.485–0.838, P = 1.20E-03). In order to examine the robustness of the IVW method, we used other three complementary analytical methods and also obtained consistent results. Conclusion The overall PD genetic risk factors did not predict AD risk, but the α-synuclein susceptibility genetic variants in PD reduce the AD risk. We believe that our findings may help to understand the association between them, which may be useful for future genetic studies for both diseases.
abstract_unstemmed	Abstract Background Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the top two common neurodegenerative diseases in elderly. Recent studies found the α-synuclein have a key role in AD. Although many clinical and pathological features between AD and PD are shared, the genetic association between them remains unclear, especially whether α-synuclein in PD genetically alters AD risk. Results We did not obtain any significant result (OR = 0.918, 95% CI: 0.782–1.076, P = 0.291) in MR analysis between PD and AD risk. In MR between α-synuclein in PD with AD risk, we only extracted rs356182 as the IV through a strict screening process. The result indicated a significant association based on IVW method (OR = 0.638, 95% CI: 0.485–0.838, P = 1.20E-03). In order to examine the robustness of the IVW method, we used other three complementary analytical methods and also obtained consistent results. Conclusion The overall PD genetic risk factors did not predict AD risk, but the α-synuclein susceptibility genetic variants in PD reduce the AD risk. We believe that our findings may help to understand the association between them, which may be useful for future genetic studies for both diseases.
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title_short	Parkinson’s disease and Alzheimer’s disease: a Mendelian randomization study
url	https://doi.org/10.1186/s12881-018-0721-7 https://doaj.org/article/3b3d5a6b4dc2498391da937cf0c57043 http://link.springer.com/article/10.1186/s12881-018-0721-7 https://doaj.org/toc/1471-2350
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Parkinson’s disease and Alzheimer’s disease: a Mendelian randomization study

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