Disease and anatomic specificity of ethanolamine plasmalogen deficiency in Alzheimer's disease brain

Brain Res. 1995 Nov 6;698(1-2):223-6. doi: 10.1016/0006-8993(95)00931-f.


A significant and selective deficiency of ethanolamine plasmalogen (PPE) relative to phosphatidylethanolamine was identified in post mortem brain samples from patients with Alzheimer's disease (AD). This lipid defect showed anatomic specificity, being more marked at a site of neurodegeneration in AD brain than in a region relatively spared by the disease (mid-temporal cortex vs. cerebellum) and disease specificity for AD: it was not observed at the primary site of neurodegeneration in Huntington's disease (caudate nucleus) nor Parkinson's disease (substantia nigra). PPE deficiency parallels an inherent tendency towards membrane bilayer instability previously detected in AD brain which is necessarily due to a change in membrane lipid composition, and which may contribute to AD pathogenesis.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Aged, 80 and over
  • Alzheimer Disease / physiopathology*
  • Caudate Nucleus / physiopathology
  • Cerebellum / pathology
  • Cerebellum / physiopathology*
  • Humans
  • Huntington Disease / pathology
  • Huntington Disease / physiopathology*
  • Middle Aged
  • Parkinson Disease / pathology
  • Parkinson Disease / physiopathology*
  • Plasmalogens / physiology*
  • Substantia Nigra / physiopathology
  • Temporal Lobe / pathology
  • Temporal Lobe / physiopathology*


  • Plasmalogens
  • phosphatidal ethanolamines