Table 1.
Summary of DMS-based metabolomics studies on Alzheimer’s disease.
| Cohort | Sample | Results | Ref. |
|---|---|---|---|
| AD (N = 22) HC (N = 18) |
serum | imbalances in the PUFA/SFA composition of phospholipids; impairments in energy metabolism, neurotransmission, fatty acid homeostasis; hyperlipidemia | [20] |
| AD (N = 22) HC (N = 18) |
serum | imbalances in the PUFA/SFA composition of phospholipids | [21] |
| AD (N = 30) HC (N = 30) |
serum | up-regulated degradation of membrane phospholipids and sphingolipids (↑ diacylglycerols, ceramides); impairments in neurotransmission | [22] |
| AD (N = 22) HC (N = 18) |
serum | impairments in membrane phospholipids (↓ PUFA, ↑diacylglycerols), homeostasis of neurotransmitter systems, nitrogen metabolism and oxidative stress | [23] |
| AD (N = 19) HC (N = 17) |
serum | abnormal phospholipid homeostasis (imbalance of PUFA/SFA, over-activation of phospholipases, oxidative stress, peroxysomal dysfunction) | [24] |
| APP × PS1 (N = 30) WT (N = 30) |
serum | impairments in phospholipid homeostasis, energy-related metabolism, oxidative stress, hyperlipidemia, hyperammonemia | [25] |
| APP × PS1 × IL4-KO (N = 7) APP × PS1 (N = 7) WT (N = 7) |
serum | up-regulated production of eicosanoids, altered metabolism of amino acids and urea cycle | [26] |
| CRND8 (N = 6) WT (N = 6) |
hippocampus | altered metabolism of arachidonic acid, carbohydrates and nucleotides | [27] |
| CRND8 (N = 6) WT (N = 6) |
cerebellum | up-regulated production of eicosanoids; altered metabolism of amino acids and nucleotides | [28] |
| APP × PS1 (N = 30) WT (N = 30) |
hippocampus, cortex, cerebellum, olfactory bulb | disturbances in the homeostasis of phospholipids, acyl-carnitines, fatty acids, nucleotides, amino acids, steroids, energy-related metabolites | [29] |
| AD young (N = 17) AD old (N = 17) MCI (N = 19) HC young (N = 20) HC old (N = 8) |
CSF, frontal cortex grey and white matter | abnormal lipid homeostasis (plasmalogens, phosphatidylethanolamines, diacylglycerols) | [30] |
| APP × PS1 (N = 30) WT (N = 30) |
liver, kidney, spleen, thymus | oxidative stress, lipid dyshomeostasis, imbalances in energy metabolism, homeostasis of amino acids and nucleotides | [31] |
| APP × PS1 (N = 10) WT (N = 10) |
urine | unidentified discriminant signals | [32] |
| AD (N = 24) HC (N = 6) APPV717F, APPsw, WT |
superior frontal cortex, superior temporal cortex, inferior parietal cortex, cerebellum | plasmalogen deficiency | [33] |
| AD (N = 17), HC (N = 5) | middle frontal gyrus, superior temporal gyrus, inferior parietal lobule, hippocampus, subiculum, entorhinal cortex | sulfatide deficiency | [34] |
| APPV717F, APPsw, WT | cortex, cerebellum | sulfatide deficiency | [35] |
| AD (N = 6) HC (N = 8) |
superior frontal gyrus | sulfatide deficiency | [36] |
| AD (N = 26) HC (N = 26) |
plasma | altered sphingolipidome | [37] |
| AD (N = 93) HC (N = 99) |
serum | authors failed to replicate the 10-metabolite panel described by Mapstone et al. [38] | [39] |
| MCI (N = 28) HC (N = 73) |
plasma | discovery of a panel of 24 metabolites mainly phospholipids and acyl-carnitines) | [40] |
| AD (N = 143) MCI (N = 145) HC (N = 153) |
plasma | impairments in phospholipid homeostasis | [41] |
| AD (N = 53) MCI (N = 33) HC (N = 35) |
plasma | impairments in phospholipid homeostasis | [42] |
| AD, MCI, HC | brain, serum | impairments in the homeostasis of phospholipids and sphingolipids | [43] |
| APP × PS1 (N = 9) WT (N = 9) |
brain, plasma | impairments in the homeostasis of phospholipids, acyl-carnitines, amino acids and polyamines | [44] |