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Plasmalogen-selective phospholipase A2 and its involvement in Alzheimer's disease.

Phospholipases A2 (PLA,, EC 3.1.1.4) represent a growing superfamily of enzymes that catalyse the hydrolysis of glycerophospholipids at the sn-2 position, to produce free fatty acids and 1-acyl lysophospholipids [ 1,2,3]. The major polyunsaturated fatty acid generated upon PLA2 activation is arachidonic acid which is the rate-limiting precursor of eicosanoid formation. The lysoglycerophospholipid either acts as a substrate for lysophospholipase or is rapidly converted to platelet activating factor (PAF) by acetyltransferase. Arachidonic acid, eicosanoids and PAF act as intracellular second messengers and participate in a variety of regulatory and inflammatory responses. Ethanolamine plasmalogens constitute a unique class of glycerophospholipids with a vinyl ether linkage at the sn-1 position of the glycerol backbone and are a major phospholipid constituent of human neural membranes. In comparison to diacylglycerophospholipids, plasmalogens have unique membrane biophysical characteristics, have a propensity to facilitate membrane fusion and are selectively hydrolysed during ischaemic and traumatic brain injuries [4,5]. Recent studies using tissue obtained post-mortem have indicated that plasmalogens are decreased in different regions of the brain from Alzheimer’s disease (AD) patients when compared with agematched controls [6,7]. This decrease in plasmalogens in AD is accompanied by a marked elevation in glycerophosphoethanolamine and