Decreased frontal cortex levels of 20:5-containing phosphatidylcholines (PtdC) in Lewy body disease with intermediate Alzheimer’s disease (LBD-I-AD), Lewy body disease with Alzheimer’s disease (LBD-AD), and Parkinson’s disease (PD) tissues.

<p>R = ratio of the peak area of the endogenous PtdC to the peak area of the internal standard (mean ±SEM). *, p < 0.01; #, p < 0.05 vs controls.</p

Abbreviated schematic presentation of sphingolipid metabolism.

<p>Gal, galactosyl; Glu, glucosyl; Lac, lactosyl; S-1-P, sphingosine-1-phosphate. Red indicates lowered levels and blue indicates increased levels observed in our study.</p

Exact masses and MS² data for reported lipids.

<p>Exact masses and MS² data for reported lipids.</p

Patient demographic and neuropathologic features of control, Lewy body disease with intermediate Alzheimer’s pathology (LBD-I-AD), Lewy body disease with Alzheimer’s pathology (LBD-AD), and Parkinson’s disease (PD) subjects.

<p>PMI (post-mortem interval).</p

Frontal cortex levels of plasmalogens in control, Lewy body disease with intermediate Alzheimer’s disease (LBD-I-AD), Lewy body disease with Alzheimer’s disease (LBD-AD), and Parkinson’s disease (PD) tissues.

<p>PlsC, choline plasmalogens; PlsE, ethanolamine plasmalogen. R = ratio of the peak area of the endogenous plasmalogen to the peak area of the internal standard (mean ±SEM). *, p < 0.05 vs controls.</p

Abbreviated schematic presentation of DAG metabolism.

<p>LPA, lysophosphatidic acid; PC, phosphatidylcholine; PG, phosphatidylglycerol; PS, phosphatidylserine; PLC, phospholipase C; PLD, phospholipase D; SMS, sphingomyelin synthase; DGK, diacylglycerol kinase. Red indicates lowered levels and blue indicates increased levels observed in our study.</p

Frontal cortex levels of diacylglycerols (DAG) and lysophosphatidic acid 16:0 (LPA) in control, Lewy body disease with intermediate Alzheimer’s disease (LBD-I-AD), Lewy body disease with Alzheimer’s disease (LBD-AD), and Parkinson’s disease (PD) tissues.

<p>R = ratio of the peak area of the endogenous lipid to the peak area of the internal standard (mean ±SEM). Analysis of PD subgroups demonstrated that DAGs were augmented in the cortex of PD subjects with no neocortical pathology (PD-1, N = 5), subjects with sparse neocortical neuritic plaques (PD-2, N = 5), and subjects with moderate to frequent neocortical neuritic plaques (PD-3, N = 5). *, p < 0.01 vs. controls; #, p < 0.05 for PD-2 vs. PD3.</p