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Membrane Instability, Plasmalogen Content, and Alzheimer's Disease
Author(s) -
Ginsberg Lionel,
Xuereb John H.,
Gershfeld Norman L.
Publication year - 1998
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1998.70062533.x
Subject(s) - plasmalogen , membrane , glycerophospholipids , chemistry , lipid bilayer , biophysics , biochemistry , alzheimer's disease , phospholipid , biology , medicine , disease
The normal stability of the cell membrane bilayer depends on its lipid composition being appropriate to the ambient (physiological) temperature, T p . Membrane lipid composition may be altered by disease such that the bilayer is only stable at a new critical temperature, T ⋆ , which may differ from T p . In Alzheimer's disease (AD) temporal cortex, a defect of lipid composition has previously been identified, namely, a decrease in the ratio of plasmalogen to nonplasmalogen ethanolamine glycerophospholipids. Furthermore, for AD temporal cortex neural membranes, T ⋆ ≪ T p , a finding confirmed in the present study in a larger series than previously, using a new method for obtaining T ⋆ . This inequality between T ⋆ and T p has been proposed as a putative contributory pathogenetic mechanism leading to membrane destabilisation in AD brain. The plasmalogen deficiency could account for the change in T ⋆ in AD, as shown by experiments where T ⋆ was measured for artificial lipid mixtures simulating brain membranes with varying plasmalogen/nonplasmalogen ratios. The critical temperature was found to be very sensitive to small alterations in plasmalogen content.