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ApoA1, ApoJ and ApoE Plasma Levels and Genotype Frequencies in Cerebral Amyloid Angiopathy.
Neuromolecular Med. 2016 Mar; 18(1):99-108.NM

Abstract

The involvement of apolipoproteins, such as the ApoE4 isoform, in Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA) highlights the fact that certain lipid carriers may participate in soluble β-amyloid (Aβ) transport. Our general aim was to characterize the soluble levels of the apolipoproteins apoE, apoA1 and apoJ/clusterin and their genotype status in patients with CAA. We analyzed the genotypes frequency of APOA1 (rs5069, rs670), CLU (rs11136000, rs1532278, rs7012010, rs9331888) and APOE (rs429358, rs7412) in a cohort of patients with CAA-associated intracerebral hemorrhage (ICH) (n = 59) and compared the results with those from hypertension-associated ICH (n = 42), AD patients (n = 73) and controls (n = 88). In a subgroup of patients, we also determined the plasma concentrations of apoE, apoA1 and apoJ/clusterin. We found increased plasma apoJ/clusterin levels in CAA patients compared to AD patients or controls after adjusting for sex and age (CAA vs. controls, p = 0.033; CAA vs. AD, p = 0.013). ApoA1 levels were not altered between groups, although a strong correlation was observed between plasma Aβ(1-40) and apoA1 among CAA patients (r = 0.583, p = 0.007). Regarding plasma apoE concentration, a robust association between circulating levels and genotype status was confirmed (p < 0.001). Whereas the APOE4 frequency was higher in AD (p < 0.001) and CAA (p = 0.013), the APOA1 and CLU genotypes were not different among groups. In the CAA cohort, the risk-linked CLU variant (C) rs11136000 was associated with white matter hyperintensities (p = 0.045) and the presence of lobar microbleeds (p = 0.023) on MRI. In summary, our findings suggest that apoA1 may act as a physiological transporter of Aβ(1-40) and that apoJ/clusterin appears to be a chaperone related to distinctive lesions in CAA brains.

Authors+Show Affiliations

Neurovascular Research Laboratory, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Pg. Vall d'Hebron 119-129, 08035, Barcelona, Spain.Neurovascular Research Laboratory, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Pg. Vall d'Hebron 119-129, 08035, Barcelona, Spain.Neurovascular Research Laboratory, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Pg. Vall d'Hebron 119-129, 08035, Barcelona, Spain.Neurovascular Research Laboratory, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Pg. Vall d'Hebron 119-129, 08035, Barcelona, Spain.Neurovascular Research Laboratory, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Pg. Vall d'Hebron 119-129, 08035, Barcelona, Spain.Department of Clinical and Molecular Genetics, Vall d'Hebron Hospital, Barcelona, Spain.Neurovascular Unit, Neurology Department, Vall d'Hebron Hospital, Barcelona, Spain.Dementia Unit, Neurology Department, Vall d'Hebron Hospital, Barcelona, Spain.Dementia Unit, Neurology Department, Vall d'Hebron Hospital, Barcelona, Spain.Neurovascular Research Laboratory, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Pg. Vall d'Hebron 119-129, 08035, Barcelona, Spain. Neurovascular Unit, Neurology Department, Vall d'Hebron Hospital, Barcelona, Spain.Neurovascular Research Laboratory, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Pg. Vall d'Hebron 119-129, 08035, Barcelona, Spain. mar.hernandez.guillamon@vhir.org.

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26661731

Citation

Montañola, Alex, et al. "ApoA1, ApoJ and ApoE Plasma Levels and Genotype Frequencies in Cerebral Amyloid Angiopathy." Neuromolecular Medicine, vol. 18, no. 1, 2016, pp. 99-108.
Montañola A, de Retana SF, López-Rueda A, et al. ApoA1, ApoJ and ApoE Plasma Levels and Genotype Frequencies in Cerebral Amyloid Angiopathy. Neuromolecular Med. 2016;18(1):99-108.
Montañola, A., de Retana, S. F., López-Rueda, A., Merino-Zamorano, C., Penalba, A., Fernández-Álvarez, P., Rodríguez-Luna, D., Malagelada, A., Pujadas, F., Montaner, J., & Hernández-Guillamon, M. (2016). ApoA1, ApoJ and ApoE Plasma Levels and Genotype Frequencies in Cerebral Amyloid Angiopathy. Neuromolecular Medicine, 18(1), 99-108. https://doi.org/10.1007/s12017-015-8381-7
Montañola A, et al. ApoA1, ApoJ and ApoE Plasma Levels and Genotype Frequencies in Cerebral Amyloid Angiopathy. Neuromolecular Med. 2016;18(1):99-108. PubMed PMID: 26661731.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - ApoA1, ApoJ and ApoE Plasma Levels and Genotype Frequencies in Cerebral Amyloid Angiopathy. AU - Montañola,Alex, AU - de Retana,Sofía Fernández, AU - López-Rueda,Antonio, AU - Merino-Zamorano,Cristina, AU - Penalba,Anna, AU - Fernández-Álvarez,Paula, AU - Rodríguez-Luna,David, AU - Malagelada,Ana, AU - Pujadas,Francesc, AU - Montaner,Joan, AU - Hernández-Guillamon,Mar, Y1 - 2015/12/14/ PY - 2015/08/14/received PY - 2015/11/17/accepted PY - 2015/12/15/entrez PY - 2015/12/15/pubmed PY - 2016/12/29/medline KW - APOA1 KW - APOE KW - APOJ KW - Alzheimer’s disease KW - CLU KW - Cerebral Amyloid Angiopathy KW - Clusterin KW - apoA1 KW - apoE KW - apoJ SP - 99 EP - 108 JF - Neuromolecular medicine JO - Neuromolecular Med. VL - 18 IS - 1 N2 - The involvement of apolipoproteins, such as the ApoE4 isoform, in Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA) highlights the fact that certain lipid carriers may participate in soluble β-amyloid (Aβ) transport. Our general aim was to characterize the soluble levels of the apolipoproteins apoE, apoA1 and apoJ/clusterin and their genotype status in patients with CAA. We analyzed the genotypes frequency of APOA1 (rs5069, rs670), CLU (rs11136000, rs1532278, rs7012010, rs9331888) and APOE (rs429358, rs7412) in a cohort of patients with CAA-associated intracerebral hemorrhage (ICH) (n = 59) and compared the results with those from hypertension-associated ICH (n = 42), AD patients (n = 73) and controls (n = 88). In a subgroup of patients, we also determined the plasma concentrations of apoE, apoA1 and apoJ/clusterin. We found increased plasma apoJ/clusterin levels in CAA patients compared to AD patients or controls after adjusting for sex and age (CAA vs. controls, p = 0.033; CAA vs. AD, p = 0.013). ApoA1 levels were not altered between groups, although a strong correlation was observed between plasma Aβ(1-40) and apoA1 among CAA patients (r = 0.583, p = 0.007). Regarding plasma apoE concentration, a robust association between circulating levels and genotype status was confirmed (p < 0.001). Whereas the APOE4 frequency was higher in AD (p < 0.001) and CAA (p = 0.013), the APOA1 and CLU genotypes were not different among groups. In the CAA cohort, the risk-linked CLU variant (C) rs11136000 was associated with white matter hyperintensities (p = 0.045) and the presence of lobar microbleeds (p = 0.023) on MRI. In summary, our findings suggest that apoA1 may act as a physiological transporter of Aβ(1-40) and that apoJ/clusterin appears to be a chaperone related to distinctive lesions in CAA brains. SN - 1559-1174 UR - https://www.unboundmedicine.com/medline/citation/26661731/ApoA1_ApoJ_and_ApoE_Plasma_Levels_and_Genotype_Frequencies_in_Cerebral_Amyloid_Angiopathy_ L2 - https://dx.doi.org/10.1007/s12017-015-8381-7 DB - PRIME DP - Unbound Medicine ER -