RT info:eu-repo/semantics/article
T1 Comparison of plasma lipoprotein composition and function in cerebral amyloid angiopathy and Alzheimer’s disease
A1 Bonaterra Pastra, Anna
A1 Fernández de Retana, Sofia
A1 Rivas Urbina, Andrea
A1 Puig, Nuria
A1 Benítez, Sonia
A1 Pancorbo, Olalla
A1 Rodríguez Luna, David
A1 Pujadas, Francesc
A1 Freijo Guerrero, María del Mar
A1 Tur, Silvia
A1 Martínez Zabaleta, Maite
A1 Cardona Portela, Pere
A1 Vera, Rocío
A1 Lebrato Hernández, Lucía
A1 Arenillas Lara, Juan Francisco
A1 Pérez Sánchez, Soledad
A1 Montaner, Joan
A1 Sánchez Quesada, Jose Luis
A1 Hernández Guillamon, Mar
K1 Alzheimer's disease
K1 Alzheimer, Enfermedad de
K1 Lipids
K1 Neurology
K1 Cerebro - Enfermedades
K1 Lípidos
K1 Proteins
K1 Proteinas
K1 3207.11 Neuropatología
AB 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.
PB MDPI
SN 2227-9059
YR 2021
FD 2021
LK https://uvadoc.uva.es/handle/10324/59857
UL https://uvadoc.uva.es/handle/10324/59857
LA eng
NO Biomedicines, 2021, Vol. 9, Nº. 1, 72
NO Producción Científica
DS UVaDOC
RD 24-nov-2024