Range |
PlsPEs out of PEs in brain ≤58%: PlsPCs out of PEs in heart ≤26% %
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Organism |
Human Homo sapiens |
Reference |
Koivuniemi A. The biophysical properties of plasmalogens originating from their unique molecular architecture. FEBS Lett. 2017 Sep591(18):2700-2713. doi: 10.1002/1873-3468.12754 p.2701 right column 2nd paragraphPubMed ID28710769
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Primary Source |
[14] Han X, Holtzman DM, McKeel DW Jr. Plasmalogen deficiency in early Alzheimer's disease subjects and in animal models: molecular characterization using electrospray ionization mass spectrometry. J Neurochem. 2001 May77(4):1168-80 [16] Gottfried EL and Rapport MM (1962) The biochemistry of plasmalogens. J Biol Chem 237, 329–333.PubMed ID11359882, 13900748
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Method |
Primary source [14] abstract: "To explore the hypothesis that alterations in ethanolamine plasmalogen may be directly related to the severity of dementia in Alzheimer's disease (AD), [investigators] performed a systematic examination of plasmalogen content in cellular membranes of gray and white matter from different regions of human subjects with a spectrum of AD clinical dementia ratings (CDR) using electrospray ionization mass spectrometry (ESI/MS)." |
Comments |
P.2701 right column 2nd paragraph: "Plasmalogens are present almost in all mammalian tissues and their average percentage is approximately 15–20% of total phospholipids [BNID 114191]. Consequently, plasmalogens can be treated as a major phospholipid component of cell membranes. They are mostly enriched in the brain, heart, skeletal muscle and kidney, the most abundant plasmalogens being ethanolamine plasmalogens (PlsPEs) and choline plasmalogens (PlsPCs) [refs 12, 15]. PlsPE species constitute up to 58% of phoshpatidylethanolamines (PEs) in human brain and PlsPCs up to 26% in human heart [primary sources]." |
Entered by |
Uri M |
ID |
114192 |