RT Journal Article
T1 Serum lipid profile among sporadic and familial forms of Parkinson's disease.
A1 Macias-Garcia, Daniel
A1 Periñan, Maria Teresa
A1 Muñoz-Delgado, Laura
A1 Jimenez-Jaraba, Maria Valle
A1 Labrador-Espinosa, Miguel Angel
A1 Jesus, Silvia
A1 Buiza-Rueda, Dolores
A1 Mendez-Del-Barrio, Carlota
A1 Adarmes-Gomez, Astrid
A1 Gomez-Garre, Pilar
A1 Mir, Pablo
K1 Parkinson's disease
K1 Cholesterol
K1 Brain
K1 Genetic Background
AB Brain cholesterol metabolism has been described as altered in Parkinson's disease (PD) patients. Serum lipid levels have been widely studied in PD with controversial results among different populations and age groups. The present study is aimed at determining if the serum lipid profile could be influenced by the genetic background of PD patients. We included 403 PD patients (342 sporadic PD patients, 30 GBA-associated PD patients, and 31 LRRK2-associated PD patients) and 654 healthy controls (HCs). Total cholesterol, HDL, LDL, and triglycerides were measured in peripheral blood. Analysis of covariance adjusting for sex and age (ANCOVA) and post hoc tests were applied to determine the differences within lipid profiles among the groups. Multivariate ANCOVA revealed significant differences among the groups within cholesterol and LDL levels. GBA-associated PD patients had significantly lower levels of total cholesterol and LDL compared to LRRK2-associated PD patients and HCs. The different serum cholesterol levels in GBA-associated PD might be related to diverse pathogenic mechanisms. Our results support the hypothesis of lipid metabolism disruption as one of the main PD pathogenic mechanisms in patients with GBA-associated PD. Further studies would be necessary to explore their clinical implications.
PB Nature Publishing Group
SN 2373-8057
YR 2021
FD 2021-07-16
LK http://hdl.handle.net/10668/18207
UL http://hdl.handle.net/10668/18207
LA en
NO Macías-García D, Periñán MT, Muñoz-Delgado L, Jimenez-Jaraba MV, Labrador-Espinosa MÁ, Jesús S, et al. Serum lipid profile among sporadic and familial forms of Parkinson's disease. NPJ Parkinsons Dis. 2021 Jul 16;7(1):59.
NO The authors thank the donors and the Hospital Universitario Virgen del Rocío-Instituto de Biomedicina de Sevilla Biobank (Andalusian Public Health System Biobank and ISCIII-Red de Biobancos PT17/0015/0041) for the human specimens used in this study. This work was supported by the Spanish Ministry of Science and Innovation [RTC2019-007150-1], the Instituto de Salud Carlos III-Fondo Europeo de Desarrollo Regional (ISCIII-FEDER) [PI14/01823, PI16/01575, PI18/01898, PI19/01576], the Consejería de Economía, Innovación, Ciencia y Empleo de la Junta de Andalucía [CVI-02526, CTS-7685], the Consejería de Salud y Bienestar Social de la Junta de Andalucía [PI-0471-2013, PE-0210-2018, PI-0459-2018, PE-0186-2019], and the Fundación Alicia Koplowitz. Pilar Gómez-Garre was supported by the “Nicolás Monardes” program [C-0048-2017] (from Andalusian Regional Ministry of Health ). Silvia Jesús was supported by the “Acción B Clínicos Investigadores” program from the Consejería de Salud y Familias de la Junta de Andalucía [B-0007-2019]. Daniel Macías-García was supported by the “Río Hortega” program [CM18/00142] from the Instituto de Salud Carlos III (ISCIII-FEDER). María Teresa Periñán was supported by the Spanish Ministry of Education , Culture and Sports [FPU16/05061]. Miguel Ángel Labrador -Espinosa is supported by University of Seville [USE-18817-A].
DS RISalud
RD Apr 16, 2025