Assessment of APOE in atypical parkinsonism syndromes
Atypical parkinsonism syndromes are a heterogeneous group of neurodegenerative disorders that include corticobasal degeneration (CBD), Lewy body dementia (LBD), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). The APOE ε4 allele is a well-established risk factor for Alzheimer...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Sabir, Marya S. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2019transfer abstract |
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| Umfang: |
5 |
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| Übergeordnetes Werk: |
Enthalten in: Rational administration sequencing of immunochemotherapy elicits powerful anti-tumor effect - Zhu, Chunqi ELSEVIER, 2021, Orlando, Fla |
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| Übergeordnetes Werk: |
volume:127 ; year:2019 ; pages:142-146 ; extent:5 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.nbd.2019.02.016 |
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ELV047171286 |
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| 245 | 1 | 0 | |a Assessment of APOE in atypical parkinsonism syndromes |
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| 520 | |a Atypical parkinsonism syndromes are a heterogeneous group of neurodegenerative disorders that include corticobasal degeneration (CBD), Lewy body dementia (LBD), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). The APOE ε4 allele is a well-established risk factor for Alzheimer's disease; however, the role of APOE in atypical parkinsonism syndromes remains controversial. To examine the associations of APOE ε4 and ε2 alleles with risk of developing these syndromes, a total of 991 pathologically-confirmed atypical parkinsonism cases were genotyped using the Illumina NeuroChip array. We also performed genotyping and logistic regression analyses to examine APOE frequency and associated risk in patients with Alzheimer's disease (n = 571) and Parkinson's disease (n = 348). APOE genotypes were compared to those from neurologically healthy controls (n = 591). We demonstrate that APOE ε4 and ε2 carriers have a significantly increased and decreased risk, respectively, of developing Alzheimer's disease (ε4: OR: 4.13, 95% CI: 3.23–5.26, p = 3.67 × 10−30; ε2: OR: 0.21, 95% CI: 0.13–0.34; p = 5.39 × 10−10) and LBD (ε4: OR: 2.94, 95% CI: 2.34–3.71, p = 6.60 × 10−20; ε2: OR = OR: 0.39, 95% CI: 0.26–0.59; p = 6.88 × 10−6). No significant associations with risk for CBD, MSA, or PSP were observed. We also show that APOE ε4 decreases survival in a dose-dependent manner in Alzheimer's disease and LBD. Taken together, this study does not provide evidence to implicate a role of APOE in the neuropathogenesis of CBD, MSA, or PSP. However, we confirm association of the APOE ε4 allele with increased risk for LBD, and importantly demonstrate that APOE ε2 reduces risk of this disease. | ||
| 520 | |a Atypical parkinsonism syndromes are a heterogeneous group of neurodegenerative disorders that include corticobasal degeneration (CBD), Lewy body dementia (LBD), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). The APOE ε4 allele is a well-established risk factor for Alzheimer's disease; however, the role of APOE in atypical parkinsonism syndromes remains controversial. To examine the associations of APOE ε4 and ε2 alleles with risk of developing these syndromes, a total of 991 pathologically-confirmed atypical parkinsonism cases were genotyped using the Illumina NeuroChip array. We also performed genotyping and logistic regression analyses to examine APOE frequency and associated risk in patients with Alzheimer's disease (n = 571) and Parkinson's disease (n = 348). APOE genotypes were compared to those from neurologically healthy controls (n = 591). We demonstrate that APOE ε4 and ε2 carriers have a significantly increased and decreased risk, respectively, of developing Alzheimer's disease (ε4: OR: 4.13, 95% CI: 3.23–5.26, p = 3.67 × 10−30; ε2: OR: 0.21, 95% CI: 0.13–0.34; p = 5.39 × 10−10) and LBD (ε4: OR: 2.94, 95% CI: 2.34–3.71, p = 6.60 × 10−20; ε2: OR = OR: 0.39, 95% CI: 0.26–0.59; p = 6.88 × 10−6). No significant associations with risk for CBD, MSA, or PSP were observed. We also show that APOE ε4 decreases survival in a dose-dependent manner in Alzheimer's disease and LBD. Taken together, this study does not provide evidence to implicate a role of APOE in the neuropathogenesis of CBD, MSA, or PSP. However, we confirm association of the APOE ε4 allele with increased risk for LBD, and importantly demonstrate that APOE ε2 reduces risk of this disease. | ||
| 700 | 1 | |a Blauwendraat, Cornelis |4 oth | |
| 700 | 1 | |a Ahmed, Sarah |4 oth | |
| 700 | 1 | |a Serrano, Geidy E. |4 oth | |
| 700 | 1 | |a Beach, Thomas G. |4 oth | |
| 700 | 1 | |a Perkins, Matthew |4 oth | |
| 700 | 1 | |a Rice, Ann C. |4 oth | |
| 700 | 1 | |a Masliah, Eliezer |4 oth | |
| 700 | 1 | |a Morris, Christopher M. |4 oth | |
| 700 | 1 | |a Pihlstrom, Lasse |4 oth | |
| 700 | 1 | |a Pantelyat, Alexander |4 oth | |
| 700 | 1 | |a Resnick, Susan M. |4 oth | |
| 700 | 1 | |a Cookson, Mark R. |4 oth | |
| 700 | 1 | |a Hernandez, Dena G. |4 oth | |
| 700 | 1 | |a Albert, Marilyn |4 oth | |
| 700 | 1 | |a Dawson, Ted M. |4 oth | |
| 700 | 1 | |a Rosenthal, Liana S. |4 oth | |
| 700 | 1 | |a Houlden, Henry |4 oth | |
| 700 | 1 | |a Pletnikova, Olga |4 oth | |
| 700 | 1 | |a Troncoso, Juan |4 oth | |
| 700 | 1 | |a Scholz, Sonja W. |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Academic Press |a Zhu, Chunqi ELSEVIER |t Rational administration sequencing of immunochemotherapy elicits powerful anti-tumor effect |d 2021 |g Orlando, Fla |w (DE-627)ELV007282540 |
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10.1016/j.nbd.2019.02.016 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000000882.pica (DE-627)ELV047171286 (ELSEVIER)S0969-9961(19)30046-4 DE-627 ger DE-627 rakwb eng 540 610 VZ 15,3 ssgn PHARM DE-84 fid 44.40 bkl 58.28 bkl Sabir, Marya S. verfasserin aut Assessment of APOE in atypical parkinsonism syndromes 2019transfer abstract 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Atypical parkinsonism syndromes are a heterogeneous group of neurodegenerative disorders that include corticobasal degeneration (CBD), Lewy body dementia (LBD), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). The APOE ε4 allele is a well-established risk factor for Alzheimer's disease; however, the role of APOE in atypical parkinsonism syndromes remains controversial. To examine the associations of APOE ε4 and ε2 alleles with risk of developing these syndromes, a total of 991 pathologically-confirmed atypical parkinsonism cases were genotyped using the Illumina NeuroChip array. We also performed genotyping and logistic regression analyses to examine APOE frequency and associated risk in patients with Alzheimer's disease (n = 571) and Parkinson's disease (n = 348). APOE genotypes were compared to those from neurologically healthy controls (n = 591). We demonstrate that APOE ε4 and ε2 carriers have a significantly increased and decreased risk, respectively, of developing Alzheimer's disease (ε4: OR: 4.13, 95% CI: 3.23–5.26, p = 3.67 × 10−30; ε2: OR: 0.21, 95% CI: 0.13–0.34; p = 5.39 × 10−10) and LBD (ε4: OR: 2.94, 95% CI: 2.34–3.71, p = 6.60 × 10−20; ε2: OR = OR: 0.39, 95% CI: 0.26–0.59; p = 6.88 × 10−6). No significant associations with risk for CBD, MSA, or PSP were observed. We also show that APOE ε4 decreases survival in a dose-dependent manner in Alzheimer's disease and LBD. Taken together, this study does not provide evidence to implicate a role of APOE in the neuropathogenesis of CBD, MSA, or PSP. However, we confirm association of the APOE ε4 allele with increased risk for LBD, and importantly demonstrate that APOE ε2 reduces risk of this disease. Atypical parkinsonism syndromes are a heterogeneous group of neurodegenerative disorders that include corticobasal degeneration (CBD), Lewy body dementia (LBD), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). The APOE ε4 allele is a well-established risk factor for Alzheimer's disease; however, the role of APOE in atypical parkinsonism syndromes remains controversial. To examine the associations of APOE ε4 and ε2 alleles with risk of developing these syndromes, a total of 991 pathologically-confirmed atypical parkinsonism cases were genotyped using the Illumina NeuroChip array. We also performed genotyping and logistic regression analyses to examine APOE frequency and associated risk in patients with Alzheimer's disease (n = 571) and Parkinson's disease (n = 348). APOE genotypes were compared to those from neurologically healthy controls (n = 591). We demonstrate that APOE ε4 and ε2 carriers have a significantly increased and decreased risk, respectively, of developing Alzheimer's disease (ε4: OR: 4.13, 95% CI: 3.23–5.26, p = 3.67 × 10−30; ε2: OR: 0.21, 95% CI: 0.13–0.34; p = 5.39 × 10−10) and LBD (ε4: OR: 2.94, 95% CI: 2.34–3.71, p = 6.60 × 10−20; ε2: OR = OR: 0.39, 95% CI: 0.26–0.59; p = 6.88 × 10−6). No significant associations with risk for CBD, MSA, or PSP were observed. We also show that APOE ε4 decreases survival in a dose-dependent manner in Alzheimer's disease and LBD. Taken together, this study does not provide evidence to implicate a role of APOE in the neuropathogenesis of CBD, MSA, or PSP. However, we confirm association of the APOE ε4 allele with increased risk for LBD, and importantly demonstrate that APOE ε2 reduces risk of this disease. Blauwendraat, Cornelis oth Ahmed, Sarah oth Serrano, Geidy E. oth Beach, Thomas G. oth Perkins, Matthew oth Rice, Ann C. oth Masliah, Eliezer oth Morris, Christopher M. oth Pihlstrom, Lasse oth Pantelyat, Alexander oth Resnick, Susan M. oth Cookson, Mark R. oth Hernandez, Dena G. oth Albert, Marilyn oth Dawson, Ted M. oth Rosenthal, Liana S. oth Houlden, Henry oth Pletnikova, Olga oth Troncoso, Juan oth Scholz, Sonja W. oth Enthalten in Academic Press Zhu, Chunqi ELSEVIER Rational administration sequencing of immunochemotherapy elicits powerful anti-tumor effect 2021 Orlando, Fla (DE-627)ELV007282540 volume:127 year:2019 pages:142-146 extent:5 https://doi.org/10.1016/j.nbd.2019.02.016 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-PHARM SSG-OLC-PHA SSG-OPC-PHA 44.40 Pharmazie Pharmazeutika VZ 58.28 Pharmazeutische Technologie VZ AR 127 2019 142-146 5 |
| spelling |
10.1016/j.nbd.2019.02.016 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000000882.pica (DE-627)ELV047171286 (ELSEVIER)S0969-9961(19)30046-4 DE-627 ger DE-627 rakwb eng 540 610 VZ 15,3 ssgn PHARM DE-84 fid 44.40 bkl 58.28 bkl Sabir, Marya S. verfasserin aut Assessment of APOE in atypical parkinsonism syndromes 2019transfer abstract 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Atypical parkinsonism syndromes are a heterogeneous group of neurodegenerative disorders that include corticobasal degeneration (CBD), Lewy body dementia (LBD), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). The APOE ε4 allele is a well-established risk factor for Alzheimer's disease; however, the role of APOE in atypical parkinsonism syndromes remains controversial. To examine the associations of APOE ε4 and ε2 alleles with risk of developing these syndromes, a total of 991 pathologically-confirmed atypical parkinsonism cases were genotyped using the Illumina NeuroChip array. We also performed genotyping and logistic regression analyses to examine APOE frequency and associated risk in patients with Alzheimer's disease (n = 571) and Parkinson's disease (n = 348). APOE genotypes were compared to those from neurologically healthy controls (n = 591). We demonstrate that APOE ε4 and ε2 carriers have a significantly increased and decreased risk, respectively, of developing Alzheimer's disease (ε4: OR: 4.13, 95% CI: 3.23–5.26, p = 3.67 × 10−30; ε2: OR: 0.21, 95% CI: 0.13–0.34; p = 5.39 × 10−10) and LBD (ε4: OR: 2.94, 95% CI: 2.34–3.71, p = 6.60 × 10−20; ε2: OR = OR: 0.39, 95% CI: 0.26–0.59; p = 6.88 × 10−6). No significant associations with risk for CBD, MSA, or PSP were observed. We also show that APOE ε4 decreases survival in a dose-dependent manner in Alzheimer's disease and LBD. Taken together, this study does not provide evidence to implicate a role of APOE in the neuropathogenesis of CBD, MSA, or PSP. However, we confirm association of the APOE ε4 allele with increased risk for LBD, and importantly demonstrate that APOE ε2 reduces risk of this disease. Atypical parkinsonism syndromes are a heterogeneous group of neurodegenerative disorders that include corticobasal degeneration (CBD), Lewy body dementia (LBD), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). The APOE ε4 allele is a well-established risk factor for Alzheimer's disease; however, the role of APOE in atypical parkinsonism syndromes remains controversial. To examine the associations of APOE ε4 and ε2 alleles with risk of developing these syndromes, a total of 991 pathologically-confirmed atypical parkinsonism cases were genotyped using the Illumina NeuroChip array. We also performed genotyping and logistic regression analyses to examine APOE frequency and associated risk in patients with Alzheimer's disease (n = 571) and Parkinson's disease (n = 348). APOE genotypes were compared to those from neurologically healthy controls (n = 591). We demonstrate that APOE ε4 and ε2 carriers have a significantly increased and decreased risk, respectively, of developing Alzheimer's disease (ε4: OR: 4.13, 95% CI: 3.23–5.26, p = 3.67 × 10−30; ε2: OR: 0.21, 95% CI: 0.13–0.34; p = 5.39 × 10−10) and LBD (ε4: OR: 2.94, 95% CI: 2.34–3.71, p = 6.60 × 10−20; ε2: OR = OR: 0.39, 95% CI: 0.26–0.59; p = 6.88 × 10−6). No significant associations with risk for CBD, MSA, or PSP were observed. We also show that APOE ε4 decreases survival in a dose-dependent manner in Alzheimer's disease and LBD. Taken together, this study does not provide evidence to implicate a role of APOE in the neuropathogenesis of CBD, MSA, or PSP. However, we confirm association of the APOE ε4 allele with increased risk for LBD, and importantly demonstrate that APOE ε2 reduces risk of this disease. Blauwendraat, Cornelis oth Ahmed, Sarah oth Serrano, Geidy E. oth Beach, Thomas G. oth Perkins, Matthew oth Rice, Ann C. oth Masliah, Eliezer oth Morris, Christopher M. oth Pihlstrom, Lasse oth Pantelyat, Alexander oth Resnick, Susan M. oth Cookson, Mark R. oth Hernandez, Dena G. oth Albert, Marilyn oth Dawson, Ted M. oth Rosenthal, Liana S. oth Houlden, Henry oth Pletnikova, Olga oth Troncoso, Juan oth Scholz, Sonja W. oth Enthalten in Academic Press Zhu, Chunqi ELSEVIER Rational administration sequencing of immunochemotherapy elicits powerful anti-tumor effect 2021 Orlando, Fla (DE-627)ELV007282540 volume:127 year:2019 pages:142-146 extent:5 https://doi.org/10.1016/j.nbd.2019.02.016 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-PHARM SSG-OLC-PHA SSG-OPC-PHA 44.40 Pharmazie Pharmazeutika VZ 58.28 Pharmazeutische Technologie VZ AR 127 2019 142-146 5 |
| allfields_unstemmed |
10.1016/j.nbd.2019.02.016 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000000882.pica (DE-627)ELV047171286 (ELSEVIER)S0969-9961(19)30046-4 DE-627 ger DE-627 rakwb eng 540 610 VZ 15,3 ssgn PHARM DE-84 fid 44.40 bkl 58.28 bkl Sabir, Marya S. verfasserin aut Assessment of APOE in atypical parkinsonism syndromes 2019transfer abstract 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Atypical parkinsonism syndromes are a heterogeneous group of neurodegenerative disorders that include corticobasal degeneration (CBD), Lewy body dementia (LBD), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). The APOE ε4 allele is a well-established risk factor for Alzheimer's disease; however, the role of APOE in atypical parkinsonism syndromes remains controversial. To examine the associations of APOE ε4 and ε2 alleles with risk of developing these syndromes, a total of 991 pathologically-confirmed atypical parkinsonism cases were genotyped using the Illumina NeuroChip array. We also performed genotyping and logistic regression analyses to examine APOE frequency and associated risk in patients with Alzheimer's disease (n = 571) and Parkinson's disease (n = 348). APOE genotypes were compared to those from neurologically healthy controls (n = 591). We demonstrate that APOE ε4 and ε2 carriers have a significantly increased and decreased risk, respectively, of developing Alzheimer's disease (ε4: OR: 4.13, 95% CI: 3.23–5.26, p = 3.67 × 10−30; ε2: OR: 0.21, 95% CI: 0.13–0.34; p = 5.39 × 10−10) and LBD (ε4: OR: 2.94, 95% CI: 2.34–3.71, p = 6.60 × 10−20; ε2: OR = OR: 0.39, 95% CI: 0.26–0.59; p = 6.88 × 10−6). No significant associations with risk for CBD, MSA, or PSP were observed. We also show that APOE ε4 decreases survival in a dose-dependent manner in Alzheimer's disease and LBD. Taken together, this study does not provide evidence to implicate a role of APOE in the neuropathogenesis of CBD, MSA, or PSP. However, we confirm association of the APOE ε4 allele with increased risk for LBD, and importantly demonstrate that APOE ε2 reduces risk of this disease. Atypical parkinsonism syndromes are a heterogeneous group of neurodegenerative disorders that include corticobasal degeneration (CBD), Lewy body dementia (LBD), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). The APOE ε4 allele is a well-established risk factor for Alzheimer's disease; however, the role of APOE in atypical parkinsonism syndromes remains controversial. To examine the associations of APOE ε4 and ε2 alleles with risk of developing these syndromes, a total of 991 pathologically-confirmed atypical parkinsonism cases were genotyped using the Illumina NeuroChip array. We also performed genotyping and logistic regression analyses to examine APOE frequency and associated risk in patients with Alzheimer's disease (n = 571) and Parkinson's disease (n = 348). APOE genotypes were compared to those from neurologically healthy controls (n = 591). We demonstrate that APOE ε4 and ε2 carriers have a significantly increased and decreased risk, respectively, of developing Alzheimer's disease (ε4: OR: 4.13, 95% CI: 3.23–5.26, p = 3.67 × 10−30; ε2: OR: 0.21, 95% CI: 0.13–0.34; p = 5.39 × 10−10) and LBD (ε4: OR: 2.94, 95% CI: 2.34–3.71, p = 6.60 × 10−20; ε2: OR = OR: 0.39, 95% CI: 0.26–0.59; p = 6.88 × 10−6). No significant associations with risk for CBD, MSA, or PSP were observed. We also show that APOE ε4 decreases survival in a dose-dependent manner in Alzheimer's disease and LBD. Taken together, this study does not provide evidence to implicate a role of APOE in the neuropathogenesis of CBD, MSA, or PSP. However, we confirm association of the APOE ε4 allele with increased risk for LBD, and importantly demonstrate that APOE ε2 reduces risk of this disease. Blauwendraat, Cornelis oth Ahmed, Sarah oth Serrano, Geidy E. oth Beach, Thomas G. oth Perkins, Matthew oth Rice, Ann C. oth Masliah, Eliezer oth Morris, Christopher M. oth Pihlstrom, Lasse oth Pantelyat, Alexander oth Resnick, Susan M. oth Cookson, Mark R. oth Hernandez, Dena G. oth Albert, Marilyn oth Dawson, Ted M. oth Rosenthal, Liana S. oth Houlden, Henry oth Pletnikova, Olga oth Troncoso, Juan oth Scholz, Sonja W. oth Enthalten in Academic Press Zhu, Chunqi ELSEVIER Rational administration sequencing of immunochemotherapy elicits powerful anti-tumor effect 2021 Orlando, Fla (DE-627)ELV007282540 volume:127 year:2019 pages:142-146 extent:5 https://doi.org/10.1016/j.nbd.2019.02.016 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-PHARM SSG-OLC-PHA SSG-OPC-PHA 44.40 Pharmazie Pharmazeutika VZ 58.28 Pharmazeutische Technologie VZ AR 127 2019 142-146 5 |
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10.1016/j.nbd.2019.02.016 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000000882.pica (DE-627)ELV047171286 (ELSEVIER)S0969-9961(19)30046-4 DE-627 ger DE-627 rakwb eng 540 610 VZ 15,3 ssgn PHARM DE-84 fid 44.40 bkl 58.28 bkl Sabir, Marya S. verfasserin aut Assessment of APOE in atypical parkinsonism syndromes 2019transfer abstract 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Atypical parkinsonism syndromes are a heterogeneous group of neurodegenerative disorders that include corticobasal degeneration (CBD), Lewy body dementia (LBD), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). The APOE ε4 allele is a well-established risk factor for Alzheimer's disease; however, the role of APOE in atypical parkinsonism syndromes remains controversial. To examine the associations of APOE ε4 and ε2 alleles with risk of developing these syndromes, a total of 991 pathologically-confirmed atypical parkinsonism cases were genotyped using the Illumina NeuroChip array. We also performed genotyping and logistic regression analyses to examine APOE frequency and associated risk in patients with Alzheimer's disease (n = 571) and Parkinson's disease (n = 348). APOE genotypes were compared to those from neurologically healthy controls (n = 591). We demonstrate that APOE ε4 and ε2 carriers have a significantly increased and decreased risk, respectively, of developing Alzheimer's disease (ε4: OR: 4.13, 95% CI: 3.23–5.26, p = 3.67 × 10−30; ε2: OR: 0.21, 95% CI: 0.13–0.34; p = 5.39 × 10−10) and LBD (ε4: OR: 2.94, 95% CI: 2.34–3.71, p = 6.60 × 10−20; ε2: OR = OR: 0.39, 95% CI: 0.26–0.59; p = 6.88 × 10−6). No significant associations with risk for CBD, MSA, or PSP were observed. We also show that APOE ε4 decreases survival in a dose-dependent manner in Alzheimer's disease and LBD. Taken together, this study does not provide evidence to implicate a role of APOE in the neuropathogenesis of CBD, MSA, or PSP. However, we confirm association of the APOE ε4 allele with increased risk for LBD, and importantly demonstrate that APOE ε2 reduces risk of this disease. Atypical parkinsonism syndromes are a heterogeneous group of neurodegenerative disorders that include corticobasal degeneration (CBD), Lewy body dementia (LBD), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). The APOE ε4 allele is a well-established risk factor for Alzheimer's disease; however, the role of APOE in atypical parkinsonism syndromes remains controversial. To examine the associations of APOE ε4 and ε2 alleles with risk of developing these syndromes, a total of 991 pathologically-confirmed atypical parkinsonism cases were genotyped using the Illumina NeuroChip array. We also performed genotyping and logistic regression analyses to examine APOE frequency and associated risk in patients with Alzheimer's disease (n = 571) and Parkinson's disease (n = 348). APOE genotypes were compared to those from neurologically healthy controls (n = 591). We demonstrate that APOE ε4 and ε2 carriers have a significantly increased and decreased risk, respectively, of developing Alzheimer's disease (ε4: OR: 4.13, 95% CI: 3.23–5.26, p = 3.67 × 10−30; ε2: OR: 0.21, 95% CI: 0.13–0.34; p = 5.39 × 10−10) and LBD (ε4: OR: 2.94, 95% CI: 2.34–3.71, p = 6.60 × 10−20; ε2: OR = OR: 0.39, 95% CI: 0.26–0.59; p = 6.88 × 10−6). No significant associations with risk for CBD, MSA, or PSP were observed. We also show that APOE ε4 decreases survival in a dose-dependent manner in Alzheimer's disease and LBD. Taken together, this study does not provide evidence to implicate a role of APOE in the neuropathogenesis of CBD, MSA, or PSP. However, we confirm association of the APOE ε4 allele with increased risk for LBD, and importantly demonstrate that APOE ε2 reduces risk of this disease. Blauwendraat, Cornelis oth Ahmed, Sarah oth Serrano, Geidy E. oth Beach, Thomas G. oth Perkins, Matthew oth Rice, Ann C. oth Masliah, Eliezer oth Morris, Christopher M. oth Pihlstrom, Lasse oth Pantelyat, Alexander oth Resnick, Susan M. oth Cookson, Mark R. oth Hernandez, Dena G. oth Albert, Marilyn oth Dawson, Ted M. oth Rosenthal, Liana S. oth Houlden, Henry oth Pletnikova, Olga oth Troncoso, Juan oth Scholz, Sonja W. oth Enthalten in Academic Press Zhu, Chunqi ELSEVIER Rational administration sequencing of immunochemotherapy elicits powerful anti-tumor effect 2021 Orlando, Fla (DE-627)ELV007282540 volume:127 year:2019 pages:142-146 extent:5 https://doi.org/10.1016/j.nbd.2019.02.016 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-PHARM SSG-OLC-PHA SSG-OPC-PHA 44.40 Pharmazie Pharmazeutika VZ 58.28 Pharmazeutische Technologie VZ AR 127 2019 142-146 5 |
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Assessment of APOE in atypical parkinsonism syndromes |
| abstract |
Atypical parkinsonism syndromes are a heterogeneous group of neurodegenerative disorders that include corticobasal degeneration (CBD), Lewy body dementia (LBD), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). The APOE ε4 allele is a well-established risk factor for Alzheimer's disease; however, the role of APOE in atypical parkinsonism syndromes remains controversial. To examine the associations of APOE ε4 and ε2 alleles with risk of developing these syndromes, a total of 991 pathologically-confirmed atypical parkinsonism cases were genotyped using the Illumina NeuroChip array. We also performed genotyping and logistic regression analyses to examine APOE frequency and associated risk in patients with Alzheimer's disease (n = 571) and Parkinson's disease (n = 348). APOE genotypes were compared to those from neurologically healthy controls (n = 591). We demonstrate that APOE ε4 and ε2 carriers have a significantly increased and decreased risk, respectively, of developing Alzheimer's disease (ε4: OR: 4.13, 95% CI: 3.23–5.26, p = 3.67 × 10−30; ε2: OR: 0.21, 95% CI: 0.13–0.34; p = 5.39 × 10−10) and LBD (ε4: OR: 2.94, 95% CI: 2.34–3.71, p = 6.60 × 10−20; ε2: OR = OR: 0.39, 95% CI: 0.26–0.59; p = 6.88 × 10−6). No significant associations with risk for CBD, MSA, or PSP were observed. We also show that APOE ε4 decreases survival in a dose-dependent manner in Alzheimer's disease and LBD. Taken together, this study does not provide evidence to implicate a role of APOE in the neuropathogenesis of CBD, MSA, or PSP. However, we confirm association of the APOE ε4 allele with increased risk for LBD, and importantly demonstrate that APOE ε2 reduces risk of this disease. |
| abstractGer |
Atypical parkinsonism syndromes are a heterogeneous group of neurodegenerative disorders that include corticobasal degeneration (CBD), Lewy body dementia (LBD), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). The APOE ε4 allele is a well-established risk factor for Alzheimer's disease; however, the role of APOE in atypical parkinsonism syndromes remains controversial. To examine the associations of APOE ε4 and ε2 alleles with risk of developing these syndromes, a total of 991 pathologically-confirmed atypical parkinsonism cases were genotyped using the Illumina NeuroChip array. We also performed genotyping and logistic regression analyses to examine APOE frequency and associated risk in patients with Alzheimer's disease (n = 571) and Parkinson's disease (n = 348). APOE genotypes were compared to those from neurologically healthy controls (n = 591). We demonstrate that APOE ε4 and ε2 carriers have a significantly increased and decreased risk, respectively, of developing Alzheimer's disease (ε4: OR: 4.13, 95% CI: 3.23–5.26, p = 3.67 × 10−30; ε2: OR: 0.21, 95% CI: 0.13–0.34; p = 5.39 × 10−10) and LBD (ε4: OR: 2.94, 95% CI: 2.34–3.71, p = 6.60 × 10−20; ε2: OR = OR: 0.39, 95% CI: 0.26–0.59; p = 6.88 × 10−6). No significant associations with risk for CBD, MSA, or PSP were observed. We also show that APOE ε4 decreases survival in a dose-dependent manner in Alzheimer's disease and LBD. Taken together, this study does not provide evidence to implicate a role of APOE in the neuropathogenesis of CBD, MSA, or PSP. However, we confirm association of the APOE ε4 allele with increased risk for LBD, and importantly demonstrate that APOE ε2 reduces risk of this disease. |
| abstract_unstemmed |
Atypical parkinsonism syndromes are a heterogeneous group of neurodegenerative disorders that include corticobasal degeneration (CBD), Lewy body dementia (LBD), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). The APOE ε4 allele is a well-established risk factor for Alzheimer's disease; however, the role of APOE in atypical parkinsonism syndromes remains controversial. To examine the associations of APOE ε4 and ε2 alleles with risk of developing these syndromes, a total of 991 pathologically-confirmed atypical parkinsonism cases were genotyped using the Illumina NeuroChip array. We also performed genotyping and logistic regression analyses to examine APOE frequency and associated risk in patients with Alzheimer's disease (n = 571) and Parkinson's disease (n = 348). APOE genotypes were compared to those from neurologically healthy controls (n = 591). We demonstrate that APOE ε4 and ε2 carriers have a significantly increased and decreased risk, respectively, of developing Alzheimer's disease (ε4: OR: 4.13, 95% CI: 3.23–5.26, p = 3.67 × 10−30; ε2: OR: 0.21, 95% CI: 0.13–0.34; p = 5.39 × 10−10) and LBD (ε4: OR: 2.94, 95% CI: 2.34–3.71, p = 6.60 × 10−20; ε2: OR = OR: 0.39, 95% CI: 0.26–0.59; p = 6.88 × 10−6). No significant associations with risk for CBD, MSA, or PSP were observed. We also show that APOE ε4 decreases survival in a dose-dependent manner in Alzheimer's disease and LBD. Taken together, this study does not provide evidence to implicate a role of APOE in the neuropathogenesis of CBD, MSA, or PSP. However, we confirm association of the APOE ε4 allele with increased risk for LBD, and importantly demonstrate that APOE ε2 reduces risk of this disease. |
| collection_details |
GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-PHARM SSG-OLC-PHA SSG-OPC-PHA |
| title_short |
Assessment of APOE in atypical parkinsonism syndromes |
| url |
https://doi.org/10.1016/j.nbd.2019.02.016 |
| remote_bool |
true |
| author2 |
Blauwendraat, Cornelis Ahmed, Sarah Serrano, Geidy E. Beach, Thomas G. Perkins, Matthew Rice, Ann C. Masliah, Eliezer Morris, Christopher M. Pihlstrom, Lasse Pantelyat, Alexander Resnick, Susan M. Cookson, Mark R. Hernandez, Dena G. Albert, Marilyn Dawson, Ted M. Rosenthal, Liana S. Houlden, Henry Pletnikova, Olga Troncoso, Juan Scholz, Sonja W. |
| author2Str |
Blauwendraat, Cornelis Ahmed, Sarah Serrano, Geidy E. Beach, Thomas G. Perkins, Matthew Rice, Ann C. Masliah, Eliezer Morris, Christopher M. Pihlstrom, Lasse Pantelyat, Alexander Resnick, Susan M. Cookson, Mark R. Hernandez, Dena G. Albert, Marilyn Dawson, Ted M. Rosenthal, Liana S. Houlden, Henry Pletnikova, Olga Troncoso, Juan Scholz, Sonja W. |
| ppnlink |
ELV007282540 |
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z |
| isOA_txt |
false |
| hochschulschrift_bool |
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| author2_role |
oth oth oth oth oth oth oth oth oth oth oth oth oth oth oth oth oth oth oth oth |
| doi_str |
10.1016/j.nbd.2019.02.016 |
| up_date |
2024-07-06T22:10:14.921Z |
| _version_ |
1803869293035651072 |
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