Abstract
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.
Highlights
Parkinson’s disease (PD) is the most common neurodegenerative disorder after Alzheimer’s disease[1]
GBA-associated PD patients (GBA-PD) showed the RESULTS Case–control study The demographic characteristics and the serum lipid profile of the lowest levels of TC and low-density lipoprotein (LDL) (178.22 ± 34.47 and 105.78 ± 29.85 mg/dl, respectively), while Leucine-rich repeat kinase 2 gene (LRRK2)-PD patients had the highest levels of both TC and LDL (213.73 ± 30.01 and 141.09 ± 30.48 mg/dl, respectively)
Regarding the serum lipid profile among both groups, serum levels of total cholesterol (TC), LDL, and triglycerides were lower in PD patients triglycerides levels than sporadic PD (sPD), GBA-PD, and LRRK2-PD
Summary
Parkinson’s disease (PD) is the most common neurodegenerative disorder after Alzheimer’s disease[1]. Other studies showed lower levels of cholesterol, low-density lipoprotein (LDL), apolipoprotein-B, and triglycerides in PD patients, suggesting a protective factor of lipids in the PD course[11,13]. In a meta-analysis of genome-wide association studies of PD, it was demonstrated that lipids and lipoproteins were involved in the pathogenic mechanisms of the disease, such as oxidative stress response or lysosomal functioning[19] They found shared genetic etiology between lipid rafts total cholesterol and triglycerides and PD. GBA-PD influence of LRRK2 and GBA in that relationship, the present study had a predominance of males (73.91%), whereas LRRK2-PD is aimed at determining whether there are differences in the showed a higher proportion of females (62.98%) These serum lipid profile between sporadic PD (sPD) and the main monogenic causes of familial PD (GBA-associated PD, GBA-PD and LRRK2-associated PD, LRRK2-PD).
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