7f0ebdf4ffc8ffc780d794cc9675ec37 pmc_33445800.pdf eef96f7245530abb72f4817e4811224524cd54c9 pmc_33445800.pdf 58ac747c091e669547c40cb034384de9785f7a675b6b43c01d5151ace0622376 pmc_33445800.pdf Title: Comparison of Plasma Lipoprotein Composition and Function in Cerebral Amyloid Angiopathy and Alzheimer’s Disease Subject: Cerebral amyloid angiopathy (CAA) refers to beta-amyloid (A) deposition in brain vessels and is clinically the main cause of lobar intracerebral hemorrhage (ICH). A can also accumulate in brain parenchyma forming neuritic plaques in Alzheimer’s disease (AD). Our study aimed to determine whether the peripheral lipid profile and lipoprotein composition are associated with cerebral beta-amyloidosis pathology and may reflect biological differences in AD and CAA. For this purpose, lipid and apolipoproteins levels were analyzed in plasma from 51 ICH-CAA patients (collected during the chronic phase of the disease), 60 AD patients, and 60 control subjects. Lipoproteins (VLDL, LDL, and HDL) were isolated and their composition and pro/antioxidant ability were determined. We observed that alterations in the lipid profile and lipoprotein composition were remarkable in the ICH-CAA group compared to control subjects, whereas the AD group presented no specific alterations compared with controls. ICH-CAA patients presented an atheroprotective profile, which consisted of lower total and LDL cholesterol levels. Plasma from chronic ICH-CAA patients also showed a redistribution of ApoC-III from HDL to VLDL and a higher ApoE/ApoC-III ratio in HDL. Whether these alterations reflect a protective response or have a causative effect on the pathology requires further investigation. Keywords: cerebral amyloid angiopathy; Alzheimer’s disease; lipoprotein composition; lipid profile; apolipoproteins Author: Anna Bonaterra-Pastra, Sofia Fernández-de-Retana, Andrea Rivas-Urbina, Núria Puig, Sònia Benítez, Olalla Pancorbo, David Rodríguez-Luna, Francesc Pujadas, Maria del Mar Freijo, Silvia Tur, Maite Martínez-Zabaleta, Pere Cardona Portela, Rocío Vera, Lucia Lebrato-Hernández, Juan F. Arenillas, Soledad Pérez-Sánchez, Joan Montaner, Jose Luis Sánchez-Quesada and Mar Hernández-Guillamon Creator: LaTeX with hyperref Producer: pdfTeX-1.40.21 CreationDate: Thu Jan 14 11:14:03 2021 CET ModDate: Fri Jan 15 03:19:45 2021 CET Tagged: no UserProperties: no Suspects: no Form: none JavaScript: no Pages: 14 Encrypted: no Page size: 595.276 x 841.89 pts (A4) Page rot: 0 File size: 500677 bytes Optimized: no PDF version: 1.7 name type encoding emb sub uni object ID ------------------------------------ ----------------- ---------------- --- --- --- --------- HCRKXL+VnURWPalladioL Type 1 Custom yes yes no 10 0 ENHFCR+EURM10 Type 1 Builtin yes yes no 15 0 KCEMJB+URWPalladioL-Ital Type 1 Custom yes yes no 19 0 NCKWYG+URWPalladioL-Bold Type 1 Custom yes yes no 24 0 QAMGDN+URWPalladioL-Roma Type 1 Custom yes yes no 28 0 FOPFJM+VnURWPalladioL-Bold Type 1 Custom yes yes no 32 0 EBFBTV+TimesNewRomanPS-BoldItalicMT Type 1C WinAnsi yes yes no 40 0 MCBCCI+SourceSansRoman-Regular Type 1C Custom yes yes no 62 0 MCBCCM+SourceSansRoman.613wght Type 1C Custom yes yes no 66 0 MCBCCO+SourceSansRoman-Bold Type 1C Custom yes yes no 70 0 FIPDAD+PalatinoLinotype,Bold TrueType WinAnsi yes yes no 87 0 FIPDAE+PalatinoLinotype CID TrueType Identity-H yes yes yes 90 0 FIPDAF+PalatinoLinotype TrueType WinAnsi yes yes no 96 0 FIPDBH+PalatinoLinotype,Italic TrueType WinAnsi yes yes no 99 0 FIPEIP+TimesNewRoman CID TrueType Identity-H yes yes yes 102 0 FIPEJA+Arial CID TrueType Identity-H yes yes yes 108 0 WTAUCZ+CMSY10 Type 1 Builtin yes yes no 117 0 WBVKDJ+URWPalladioL-BoldItal Type 1 Custom yes yes no 124 0 Jhove (Rel. 1.22.1, 2019-04-17) Date: 2021-03-03 02:21:13 CET RepresentationInformation: pmc_33445800.pdf ReportingModule: PDF-hul, Rel. 1.12.1 (2019-04-17) LastModified: 2021-02-15 03:35:58 CET Size: 500677 Format: PDF Version: 1.7 Status: Well-Formed and valid SignatureMatches: PDF-hul MIMEtype: application/pdf PDFMetadata: Objects: 398 FreeObjects: 1 IncrementalUpdates: 0 DocumentCatalog: PageLayout: SinglePage PageMode: UseNone Outlines: Item: Title: Introduction Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@13c27452 Item: Title: Experimental Section Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@262b2c86 Children: Item: Title: Study Population Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@371a67ec Item: Title: Plasma Determinations Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@5ed828d Item: Title: Lipoprotein Composition Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@50d0686 Item: Title: LDL and HDL Susceptibility to Oxidation Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@7a3d45bd Item: Title: Antioxidant Capacity of HDL Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@1e7c7811 Item: Title: Statistical Analysis Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@77ec78b9 Item: Title: Results Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@1a3869f4 Children: Item: Title: Lipid Profile Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@a38d7a3 Item: Title: Prevalence of ApoE Genotypes Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@77f99a05 Item: Title: Lipoprotein Composition Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@63440df3 Item: Title: Apolipoprotein J Content in Lipoproteins Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@3aeaafa6 Item: Title: Lipoprotein Size and Oxidation-Related Functions Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@76a3e297 Item: Title: Discussion Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@4d3167f4 Item: Title: Conclusions Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@ed9d034 Item: Title: References Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@6121c9d6 Info: Title: Comparison of Plasma Lipoprotein Composition and Function in Cerebral Amyloid Angiopathy and Alzheimer’s Disease Author: Anna Bonaterra-Pastra, Sofia Fernández-de-Retana, Andrea Rivas-Urbina, Núria Puig, Sònia Benítez, Olalla Pancorbo, David Rodríguez-Luna, Francesc Pujadas, Maria del Mar Freijo, Silvia Tur, Maite Martínez-Zabaleta, Pere Cardona Portela, Rocío Vera, Lucia Lebrato-Hernández, Juan F. Arenillas, Soledad Pérez-Sánchez, Joan Montaner, Jose Luis Sánchez-Quesada and Mar Hernández-Guillamon Subject: Cerebral amyloid angiopathy (CAA) refers to beta-amyloid (A) deposition in brain vessels and is clinically the main cause of lobar intracerebral hemorrhage (ICH). A can also accumulate in brain parenchyma forming neuritic plaques in Alzheimer’s disease (AD). Our study aimed to determine whether the peripheral lipid profile and lipoprotein composition are associated with cerebral beta-amyloidosis pathology and may reflect biological differences in AD and CAA. For this purpose, lipid and apolipoproteins levels were analyzed in plasma from 51 ICH-CAA patients (collected during the chronic phase of the disease), 60 AD patients, and 60 control subjects. Lipoproteins (VLDL, LDL, and HDL) were isolated and their composition and pro/antioxidant ability were determined. We observed that alterations in the lipid profile and lipoprotein composition were remarkable in the ICH-CAA group compared to control subjects, whereas the AD group presented no specific alterations compared with controls. ICH-CAA patients presented an atheroprotective profile, which consisted of lower total and LDL cholesterol levels. Plasma from chronic ICH-CAA patients also showed a redistribution of ApoC-III from HDL to VLDL and a higher ApoE/ApoC-III ratio in HDL. Whether these alterations reflect a protective response or have a causative effect on the pathology requires further investigation. 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