Comparison of plasma lipoprotein composition and function in cerebral amyloid angiopathy and Alzheimer's disease

Cerebral amyloid angiopathy (CAA) refers to beta-amyloid (Aβ) deposition in brain vessels and is clinically the main cause of lobar intracerebral hemorrhage (ICH). Aβ can also accumulate in brain parenchyma forming neuritic plaques in Alzheimer's disease (AD). Our study aimed to determine wheth...

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Autores: Bonaterra-Pastra, Anna|||0000-0002-1480-622X, Fernández-de-Retana, Sofía|||0000-0002-6350-8640, Rivas-Urbina, Andrea|||0000-0002-0111-0477, Puig Grifol, Núria|||0000-0002-4699-3162, Benitez, Sonia|||0000-0003-3565-0743, Pancorbo, Olalla|||0000-0003-3240-4862, Rodriguez-Luna, David|||0000-0001-8053-4536, Pujadas, Francesc|||0000-0003-3569-2601, Freijo, Maria del Mar, Tur, Silvia, Martinez Zabaleta, Maite, Cardona, Pere-Joan|||0000-0001-5623-7873, Vera, Rocío, Lebrato-Hernández, Lucia|||0000-0002-3541-0697, Arenillas, Juan F.|||0000-0001-7464-6101, Pérez-Sánchez, Soledad|||0000-0002-8940-9763, Montaner, Joan|||0000-0003-4845-2279, Sánchez Quesada, José Luis|||0000-0003-0224-591X, Hernandez Guillamon, Maria Mar|||0000-0001-8844-0091
Tipo de recurso: artículo
Fecha de publicación:2021
País:España
Institución:Universitat Autònoma de Barcelona
Repositorio:Dipòsit Digital de Documents de la UAB
Idioma:inglés
OAI Identifier:oai:ddd.uab.cat:235977
Acceso en línea:https://ddd.uab.cat/record/235977
https://dx.doi.org/urn:doi:10.3390/biomedicines9010072
Access Level:acceso abierto
Palabra clave:Cerebral amyloid angiopathy
Alzheimer's disease
Lipoprotein composition
Lipid profile
Apolipoproteins
Descripción
Sumario:Cerebral amyloid angiopathy (CAA) refers to beta-amyloid (Aβ) deposition in brain vessels and is clinically the main cause of lobar intracerebral hemorrhage (ICH). Aβ 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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