ABSTRACT
Research into biochemical processes affecting membrane composition and fluidity have generated models that fit relatively well in both the neurodevelopmental hypotheses of schizophrenia and the neurodegenerative mechanisms of dementia. Data from the late 1980s suggesting increased phospholipase A2 (PLA2) activity in schizophrenia [1,2], and decreased in Alzheimer’s disease [3,4], have been replicated by several groups [5,6]. Abnormalities of PLA2 metabolism have also been described in other neuropsychiatric diseases such as multiple sclerosis [7] and temporal-lobe epilepsy [8,9].
