Bee Venom Soluble Phospholipase A2 Exerts Neuroprotective Effects in a Lipopolysaccharide-Induced Mouse Model of Alzheimer's Disease <i>via</i> Inhibition of Nuclear Factor-Kappa B.
Arachidonic acid (AA) and specific isoforms of phospholipase A(2) (PLA(2)) appear to be critical mediators in amyloid-beta (Abeta)-induced pathogenesis, leading to learning, memory, and behavioral impairments in mouse models of AD.
Investigating the metabolic and signaling pathways involving Abeta NADPH oxidase and PLA(2) can help understand the mechanisms underlying the neurodegenerative effects of oxidative stress in AD.
The use of positive modulators of PLA2 (especially of cPLA2 and iPLA2) or supplementation with dietary lipid compounds (e.g., arachidonic acid) in combination with cognitive training could be a valuable therapeutic strategy for cognitive enhancement in early-stage AD.
This review addresses some current ideas concerning how brain PLA2 and brain PGs are early and key players in acute neural trauma and in brain-cell damage associated with chronic neurodegenerative diseases such as AD.