TABLE 4.
Summary of GPs in CSF fractions and their alteration in clinical groups
| CSF | CH (n = 70) | MCI (n = 40) | LOAD (n = 29) |
| SF fraction | PC >>> PE > LPC > NAPE > PS > PAF_LL > xPE | PC (↓) | PC (↓↓) |
| LPC/PC (↑↑) | PE (↓↓) | ||
| PE and PS enriched with PUFA | PC(38a:5) (↓↓) | PS (↓↓) | |
| PC(38a:6) (↓↓) | LPC/PC (↑) | ||
| PS(38a:6) (↓↓) | 7 PC speciesa (↓↓) | ||
| PE (40p:4/40e:5) (↓↓) | |||
| NP fraction | PC >> xPE > NAPE> LPC > PE > PAF_LL, [PS(ND)] | PC and PE (↓) | LPC (↑) |
| Lipid enriched with SAFA, MUFA, PUFA | PC(32a:0) (↓↓) | xPE coelutes with NAPE (↑↑) | |
| PLA2 activity | Increased (↑) | Increased (↑↑) | |
| Interpretation | i) NP and SF rich in GPs that differ in distribution between these fractions | i) Increased GP lipolysis and oxidation | i) Breakdown of lipids, |
| ii) Reflects interstitial fluid and membrane metabolism in normal aging | ii) Early evidence of neuroinflammation | ii) Enzymatic lipolysis | |
| iii) Evidence of extensive inflammation |
We recruited CH, MCI, and LOAD study participants and fractionated their lumbar CSF into SF and NP fractions. Levels of GP were reliably detected using positive ion ESI and were quantified for the CH population (PI, PG, PA were not measured). Their direction of alterations within clinical groups and pathological significance in each clinical group are shown. Labels for GP levels in CSF fractions and the alterations in GPs and PLA2 activity in clinical groups: >, greater than; >> much greater than; >>> much more greater than; ↑, increased compared with CH; ↑↑, significantly increased compared with CH; ↓, decreased compared with CH; ↓↓ significantly decreased compared with CH. SAFA, saturated fatty acid; MUFA, monounsaturated fatty acid; ND, not determined.
Seven PC species include 32a:0, 34a:1, 34p:0/34e:1, 36a:0/38p:6, 36a:1, 38a:5, and 38a:6.