Phosphoethanolamine and ethanolamine are decreased in Alzheimer's disease and Huntington's disease.
Measurements of both phosphoethanolamine (PEA) and ethanolamine (EA) were made in postmortem brain samples from patients with Alzheimer's disease (AD) and Huntington's disease (HD) using high-performance liquid chromatography with electrochemical detection. In AD levels of PEA were significantly reduced by 64% in temporal cortex, 48% in frontal cortex and 40% in hippocampus. In HD concentrations of PEA were significantly reduced by 76% in the caudate, 53% in putamen and 48% in the nucleus accumbens. EA concentrations showed similar but smaller reductions in both diseases. Both PEA and EA are involved in phospholipid metabolism and can be released with depolarizing stimuli in some circumstances. Since two diverse neuropathologic processes can result in depleted levels of both amines in their respective regions of pathologic predilection, it is likely that the depletions accompany neuronal death.
D000368:Aged; D000544:Alzheimer Disease / Q000378:metabolism*; D001921:Brain / Q000378:metabolism*; D002540:Cerebral Cortex / Q000378:metabolism; D002851:Chromatography, High Pressure Liquid; D019856:Ethanolamine; D004983:Ethanolamines / Q000378:metabolism*; D006624:Hippocampus / Q000378:metabolism; D006801:Humans; D006816:Huntington Disease / Q000378:metabolism*; D008032:Limbic System / Q000378:metabolism; D008875:Middle Aged
D004983:Ethanolamines; D019856:Ethanolamine; C005448:phosphorylethanolamine