Genetic and Epigenetic Architecture of Alzheimer’s Dementia

Abstract Alzheimer’s disease (AD) is the most common neurodegenerative disease, affecting up to 5 % of the population over 65 years old. It is characterized by the accumulation of amyloid-β peptide and aggregation of hyperphosphorylated tau protein. Mutations in pivotal genes (APP, PSEN1, and PSEN2)...
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Gespeichert in:

Autor*in:	Cervera-Carles, Laura [verfasserIn] Clarimón, Jordi [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2016

Schlagwörter:	Alzheimer’s disease Genetic risk variants Epigenetic marks Mendelian genes

Übergeordnetes Werk:	Enthalten in: Current genetic medicine reports - New York, NY : Springer, 2013, 4(2016), 1 vom: 11. Feb., Seite 7-15
Übergeordnetes Werk:	volume:4 ; year:2016 ; number:1 ; day:11 ; month:02 ; pages:7-15

Links:	Volltext

DOI / URN:	10.1007/s40142-016-0086-1

Katalog-ID:	SPR033081077

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520			\|a Abstract Alzheimer’s disease (AD) is the most common neurodegenerative disease, affecting up to 5 % of the population over 65 years old. It is characterized by the accumulation of amyloid-β peptide and aggregation of hyperphosphorylated tau protein. Mutations in pivotal genes (APP, PSEN1, and PSEN2) result in the autosomal dominant form of the disease; however, the genetic cause of the majority of cases remains unexplained. Advances in genomic techniques have allowed the discovery of common variants that influence susceptibility to AD. In addition, low-frequency and rare variants in a small number of genes have emerged as important contributors of disease risk. Recent studies have focused on the epigenetic changes in affected individuals, such as DNA methylation patterns or microRNA levels, highlighting the possible involvement of these mechanisms in the etiology of AD. Here we review the known genetic and epigenetic factors underlying AD, emphasizing the molecular networks that appear to be fundamental players in its etiology.
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allfields	10.1007/s40142-016-0086-1 doi (DE-627)SPR033081077 (SPR)s40142-016-0086-1-e DE-627 ger DE-627 rakwb eng 610 ASE Cervera-Carles, Laura verfasserin aut Genetic and Epigenetic Architecture of Alzheimer’s Dementia 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Alzheimer’s disease (AD) is the most common neurodegenerative disease, affecting up to 5 % of the population over 65 years old. It is characterized by the accumulation of amyloid-β peptide and aggregation of hyperphosphorylated tau protein. Mutations in pivotal genes (APP, PSEN1, and PSEN2) result in the autosomal dominant form of the disease; however, the genetic cause of the majority of cases remains unexplained. Advances in genomic techniques have allowed the discovery of common variants that influence susceptibility to AD. In addition, low-frequency and rare variants in a small number of genes have emerged as important contributors of disease risk. Recent studies have focused on the epigenetic changes in affected individuals, such as DNA methylation patterns or microRNA levels, highlighting the possible involvement of these mechanisms in the etiology of AD. Here we review the known genetic and epigenetic factors underlying AD, emphasizing the molecular networks that appear to be fundamental players in its etiology. Alzheimer’s disease (dpeaa)DE-He213 Genetic risk variants (dpeaa)DE-He213 Epigenetic marks (dpeaa)DE-He213 Mendelian genes (dpeaa)DE-He213 Clarimón, Jordi verfasserin aut Enthalten in Current genetic medicine reports New York, NY : Springer, 2013 4(2016), 1 vom: 11. Feb., Seite 7-15 (DE-627)746702345 (DE-600)2716158-4 2167-4876 nnns volume:4 year:2016 number:1 day:11 month:02 pages:7-15 https://dx.doi.org/10.1007/s40142-016-0086-1 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 4 2016 1 11 02 7-15
spelling	10.1007/s40142-016-0086-1 doi (DE-627)SPR033081077 (SPR)s40142-016-0086-1-e DE-627 ger DE-627 rakwb eng 610 ASE Cervera-Carles, Laura verfasserin aut Genetic and Epigenetic Architecture of Alzheimer’s Dementia 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Alzheimer’s disease (AD) is the most common neurodegenerative disease, affecting up to 5 % of the population over 65 years old. It is characterized by the accumulation of amyloid-β peptide and aggregation of hyperphosphorylated tau protein. Mutations in pivotal genes (APP, PSEN1, and PSEN2) result in the autosomal dominant form of the disease; however, the genetic cause of the majority of cases remains unexplained. Advances in genomic techniques have allowed the discovery of common variants that influence susceptibility to AD. In addition, low-frequency and rare variants in a small number of genes have emerged as important contributors of disease risk. Recent studies have focused on the epigenetic changes in affected individuals, such as DNA methylation patterns or microRNA levels, highlighting the possible involvement of these mechanisms in the etiology of AD. Here we review the known genetic and epigenetic factors underlying AD, emphasizing the molecular networks that appear to be fundamental players in its etiology. Alzheimer’s disease (dpeaa)DE-He213 Genetic risk variants (dpeaa)DE-He213 Epigenetic marks (dpeaa)DE-He213 Mendelian genes (dpeaa)DE-He213 Clarimón, Jordi verfasserin aut Enthalten in Current genetic medicine reports New York, NY : Springer, 2013 4(2016), 1 vom: 11. Feb., Seite 7-15 (DE-627)746702345 (DE-600)2716158-4 2167-4876 nnns volume:4 year:2016 number:1 day:11 month:02 pages:7-15 https://dx.doi.org/10.1007/s40142-016-0086-1 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 4 2016 1 11 02 7-15
allfields_unstemmed	10.1007/s40142-016-0086-1 doi (DE-627)SPR033081077 (SPR)s40142-016-0086-1-e DE-627 ger DE-627 rakwb eng 610 ASE Cervera-Carles, Laura verfasserin aut Genetic and Epigenetic Architecture of Alzheimer’s Dementia 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Alzheimer’s disease (AD) is the most common neurodegenerative disease, affecting up to 5 % of the population over 65 years old. It is characterized by the accumulation of amyloid-β peptide and aggregation of hyperphosphorylated tau protein. Mutations in pivotal genes (APP, PSEN1, and PSEN2) result in the autosomal dominant form of the disease; however, the genetic cause of the majority of cases remains unexplained. Advances in genomic techniques have allowed the discovery of common variants that influence susceptibility to AD. In addition, low-frequency and rare variants in a small number of genes have emerged as important contributors of disease risk. Recent studies have focused on the epigenetic changes in affected individuals, such as DNA methylation patterns or microRNA levels, highlighting the possible involvement of these mechanisms in the etiology of AD. Here we review the known genetic and epigenetic factors underlying AD, emphasizing the molecular networks that appear to be fundamental players in its etiology. Alzheimer’s disease (dpeaa)DE-He213 Genetic risk variants (dpeaa)DE-He213 Epigenetic marks (dpeaa)DE-He213 Mendelian genes (dpeaa)DE-He213 Clarimón, Jordi verfasserin aut Enthalten in Current genetic medicine reports New York, NY : Springer, 2013 4(2016), 1 vom: 11. Feb., Seite 7-15 (DE-627)746702345 (DE-600)2716158-4 2167-4876 nnns volume:4 year:2016 number:1 day:11 month:02 pages:7-15 https://dx.doi.org/10.1007/s40142-016-0086-1 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 4 2016 1 11 02 7-15
allfieldsGer	10.1007/s40142-016-0086-1 doi (DE-627)SPR033081077 (SPR)s40142-016-0086-1-e DE-627 ger DE-627 rakwb eng 610 ASE Cervera-Carles, Laura verfasserin aut Genetic and Epigenetic Architecture of Alzheimer’s Dementia 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Alzheimer’s disease (AD) is the most common neurodegenerative disease, affecting up to 5 % of the population over 65 years old. It is characterized by the accumulation of amyloid-β peptide and aggregation of hyperphosphorylated tau protein. Mutations in pivotal genes (APP, PSEN1, and PSEN2) result in the autosomal dominant form of the disease; however, the genetic cause of the majority of cases remains unexplained. Advances in genomic techniques have allowed the discovery of common variants that influence susceptibility to AD. In addition, low-frequency and rare variants in a small number of genes have emerged as important contributors of disease risk. Recent studies have focused on the epigenetic changes in affected individuals, such as DNA methylation patterns or microRNA levels, highlighting the possible involvement of these mechanisms in the etiology of AD. Here we review the known genetic and epigenetic factors underlying AD, emphasizing the molecular networks that appear to be fundamental players in its etiology. Alzheimer’s disease (dpeaa)DE-He213 Genetic risk variants (dpeaa)DE-He213 Epigenetic marks (dpeaa)DE-He213 Mendelian genes (dpeaa)DE-He213 Clarimón, Jordi verfasserin aut Enthalten in Current genetic medicine reports New York, NY : Springer, 2013 4(2016), 1 vom: 11. Feb., Seite 7-15 (DE-627)746702345 (DE-600)2716158-4 2167-4876 nnns volume:4 year:2016 number:1 day:11 month:02 pages:7-15 https://dx.doi.org/10.1007/s40142-016-0086-1 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 4 2016 1 11 02 7-15
allfieldsSound	10.1007/s40142-016-0086-1 doi (DE-627)SPR033081077 (SPR)s40142-016-0086-1-e DE-627 ger DE-627 rakwb eng 610 ASE Cervera-Carles, Laura verfasserin aut Genetic and Epigenetic Architecture of Alzheimer’s Dementia 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Alzheimer’s disease (AD) is the most common neurodegenerative disease, affecting up to 5 % of the population over 65 years old. It is characterized by the accumulation of amyloid-β peptide and aggregation of hyperphosphorylated tau protein. Mutations in pivotal genes (APP, PSEN1, and PSEN2) result in the autosomal dominant form of the disease; however, the genetic cause of the majority of cases remains unexplained. Advances in genomic techniques have allowed the discovery of common variants that influence susceptibility to AD. In addition, low-frequency and rare variants in a small number of genes have emerged as important contributors of disease risk. Recent studies have focused on the epigenetic changes in affected individuals, such as DNA methylation patterns or microRNA levels, highlighting the possible involvement of these mechanisms in the etiology of AD. Here we review the known genetic and epigenetic factors underlying AD, emphasizing the molecular networks that appear to be fundamental players in its etiology. Alzheimer’s disease (dpeaa)DE-He213 Genetic risk variants (dpeaa)DE-He213 Epigenetic marks (dpeaa)DE-He213 Mendelian genes (dpeaa)DE-He213 Clarimón, Jordi verfasserin aut Enthalten in Current genetic medicine reports New York, NY : Springer, 2013 4(2016), 1 vom: 11. Feb., Seite 7-15 (DE-627)746702345 (DE-600)2716158-4 2167-4876 nnns volume:4 year:2016 number:1 day:11 month:02 pages:7-15 https://dx.doi.org/10.1007/s40142-016-0086-1 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 4 2016 1 11 02 7-15
language	English
source	Enthalten in Current genetic medicine reports 4(2016), 1 vom: 11. Feb., Seite 7-15 volume:4 year:2016 number:1 day:11 month:02 pages:7-15
sourceStr	Enthalten in Current genetic medicine reports 4(2016), 1 vom: 11. Feb., Seite 7-15 volume:4 year:2016 number:1 day:11 month:02 pages:7-15
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Alzheimer’s disease Genetic risk variants Epigenetic marks Mendelian genes
dewey-raw	610
isfreeaccess_bool	false
container_title	Current genetic medicine reports
authorswithroles_txt_mv	Cervera-Carles, Laura @@aut@@ Clarimón, Jordi @@aut@@
publishDateDaySort_date	2016-02-11T00:00:00Z
hierarchy_top_id	746702345
dewey-sort	3610
id	SPR033081077
language_de	englisch
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author	Cervera-Carles, Laura
spellingShingle	Cervera-Carles, Laura ddc 610 misc Alzheimer’s disease misc Genetic risk variants misc Epigenetic marks misc Mendelian genes Genetic and Epigenetic Architecture of Alzheimer’s Dementia
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topic_title	610 ASE Genetic and Epigenetic Architecture of Alzheimer’s Dementia Alzheimer’s disease (dpeaa)DE-He213 Genetic risk variants (dpeaa)DE-He213 Epigenetic marks (dpeaa)DE-He213 Mendelian genes (dpeaa)DE-He213
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title	Genetic and Epigenetic Architecture of Alzheimer’s Dementia
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title_full	Genetic and Epigenetic Architecture of Alzheimer’s Dementia
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author_browse	Cervera-Carles, Laura Clarimón, Jordi
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title_sort	genetic and epigenetic architecture of alzheimer’s dementia
title_auth	Genetic and Epigenetic Architecture of Alzheimer’s Dementia
abstract	Abstract Alzheimer’s disease (AD) is the most common neurodegenerative disease, affecting up to 5 % of the population over 65 years old. It is characterized by the accumulation of amyloid-β peptide and aggregation of hyperphosphorylated tau protein. Mutations in pivotal genes (APP, PSEN1, and PSEN2) result in the autosomal dominant form of the disease; however, the genetic cause of the majority of cases remains unexplained. Advances in genomic techniques have allowed the discovery of common variants that influence susceptibility to AD. In addition, low-frequency and rare variants in a small number of genes have emerged as important contributors of disease risk. Recent studies have focused on the epigenetic changes in affected individuals, such as DNA methylation patterns or microRNA levels, highlighting the possible involvement of these mechanisms in the etiology of AD. Here we review the known genetic and epigenetic factors underlying AD, emphasizing the molecular networks that appear to be fundamental players in its etiology.
abstractGer	Abstract Alzheimer’s disease (AD) is the most common neurodegenerative disease, affecting up to 5 % of the population over 65 years old. It is characterized by the accumulation of amyloid-β peptide and aggregation of hyperphosphorylated tau protein. Mutations in pivotal genes (APP, PSEN1, and PSEN2) result in the autosomal dominant form of the disease; however, the genetic cause of the majority of cases remains unexplained. Advances in genomic techniques have allowed the discovery of common variants that influence susceptibility to AD. In addition, low-frequency and rare variants in a small number of genes have emerged as important contributors of disease risk. Recent studies have focused on the epigenetic changes in affected individuals, such as DNA methylation patterns or microRNA levels, highlighting the possible involvement of these mechanisms in the etiology of AD. Here we review the known genetic and epigenetic factors underlying AD, emphasizing the molecular networks that appear to be fundamental players in its etiology.
abstract_unstemmed	Abstract Alzheimer’s disease (AD) is the most common neurodegenerative disease, affecting up to 5 % of the population over 65 years old. It is characterized by the accumulation of amyloid-β peptide and aggregation of hyperphosphorylated tau protein. Mutations in pivotal genes (APP, PSEN1, and PSEN2) result in the autosomal dominant form of the disease; however, the genetic cause of the majority of cases remains unexplained. Advances in genomic techniques have allowed the discovery of common variants that influence susceptibility to AD. In addition, low-frequency and rare variants in a small number of genes have emerged as important contributors of disease risk. Recent studies have focused on the epigenetic changes in affected individuals, such as DNA methylation patterns or microRNA levels, highlighting the possible involvement of these mechanisms in the etiology of AD. Here we review the known genetic and epigenetic factors underlying AD, emphasizing the molecular networks that appear to be fundamental players in its etiology.
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title_short	Genetic and Epigenetic Architecture of Alzheimer’s Dementia
url	https://dx.doi.org/10.1007/s40142-016-0086-1
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doi_str	10.1007/s40142-016-0086-1
up_date	2024-07-03T16:30:54.637Z
_version_	1803576152880578562
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Genetic and Epigenetic Architecture of Alzheimer’s Dementia

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