Among the glycerophospholipids, phospathidylcholines (PCs) were significantly decreased in the PD+/LRRK2+ or PD-/LRRK2+ compared to the other groups under study (Figure and Table ). A significant decrease of PC 14:0_18:2 was observed in the PD+/LRRK2+ compared with the PD-/LRRK2+ and iPD groups. PCs are the most abundant glycerophospholipids in membranes and are involved in the control of inflammation, neuronal differentiation and cholesterol hom eostasis , . Thus, a decrease in PCs may contribute to the neuroinflammation and disease progression , as previously suggested . In contrast, some lysophosphatidylcholines (LPCs), breakdown products of PCs, were significantly elevated in the PD+/LRRK2+ group, including LPC 18:1 and LPC 16:0 (Figure ). This is in line with a previous study , suggesting that alterations in LPCs serve as markers of mitochondrial dysfunction, neuroinflammation and oxidative stress processes. Additionally, lysophosphatidylethanolamines (LPEs), LPE 18:0 and LPE O-18:1 (Figure ), were significantly elevated in the PD+/LRRK2+ group compared with the control group. This in contrast with previous studies performed in plasma and serum of iPD participants, which found decreased levels of LPE with the advance of the disease. Thus, it would be interesting to check further whether this alteration is specific to patients carrying LRRK2 pathogenic variants. Previous studies have shown that the BPS exposure in adipocytes and macrophages induce lipidome changes including increased levels of PCs, LPCs, and LPEs. The quantitative analysis of BAs in serum did not reveal any statistically significant differences (Table ), which is in contrast with recent work on Alzheimer's disease progression in cerebrospinal fluid (CSF) samples . However, non-significant higher trends of the neuroprotective BAs chenodeoxycholic acid (CDCA), and ursodeoxycholic acid (UDCA) were observed in PD-/LRRK2+ in comparison to the PD groups (Figure ). Higher but non-significant trends of the cytotoxic BA deoxycholic acid (DCA) were also observed in the PD-/LRRK2+ group (Figure ). Previous research has reported elevated levels of secondary cytotoxic BAs in PD, including DCA and lithocholic acid, correlated with an increase in BA-metabolizing bacteria , . Thus, the non-significant higher trends of BAs found in the PD-/LRRK2+ and iPD groups may be explained by gut microbiome dysbiosis, as the gut microbiota metabolize the primary BAs to produce secondary BAs such as DCA . However, this was not investigated further here due to the lack of significance. Since BAs are crucial signaling molecules and key modulators of metabolism and immune homeostasis , investigating BAs in future studies with larger sample sizes could provide additional insights.