Search for the Causes of Schizophrenia 1995
DOI: 10.1007/978-3-642-79429-2_13
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Increased Breakdown of Membrane Phospholipids in Schizophrenia: Implications for the Hypofrontality Hypothesis

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Cited by 8 publications
(3 citation statements)
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“…Based on these studies, antioxidative enzymatic activity is decreased (Raffa et al, 2009;O'Donnell, 2012;Al-Asmari and Khan, 2014), and membrane phospholipid breakdown is accelerated in patients with schizophrenia (Horrobin, 1996). Oxidative damage to membranes has been shown to occur in patients with schizophrenia by demonstration of increased phospholipase A2 levels as the key enzyme in lipid metabolism, decreased membrane phospholipids, and enhanced levels of lipid peroxidation products (Gattaz et al, 1994). On the other hand, growing evidence has recently clarified the benefits of PPARγ agonists in attenuating oxidative stress disturbances (Qi et al, 2010).…”
Section: Pioglitazone and Oxidative Stressmentioning
confidence: 99%
“…Based on these studies, antioxidative enzymatic activity is decreased (Raffa et al, 2009;O'Donnell, 2012;Al-Asmari and Khan, 2014), and membrane phospholipid breakdown is accelerated in patients with schizophrenia (Horrobin, 1996). Oxidative damage to membranes has been shown to occur in patients with schizophrenia by demonstration of increased phospholipase A2 levels as the key enzyme in lipid metabolism, decreased membrane phospholipids, and enhanced levels of lipid peroxidation products (Gattaz et al, 1994). On the other hand, growing evidence has recently clarified the benefits of PPARγ agonists in attenuating oxidative stress disturbances (Qi et al, 2010).…”
Section: Pioglitazone and Oxidative Stressmentioning
confidence: 99%
“…Increased activity of PLA, changes in membrane integrity together with compromised energy metabolism, accumulation of ROS and abnormal signal transduction may be associated with neurodegeneration in AD. Studies on phospholipid metabolism in the brains of patients with schizophrenia have also demonstrated a reduced phosphatidylcholine mass in neural membranes, elevated PLA, activity and abnormal phospholipid metabolism [23,24]. subsequent function is derived primarily from the effects of restricted n-3 essential fatty acid (EFA) availability either due to maternal dietary deprivation in animal models, or due to preterm birth in human infants.…”
Section: Physicochernical and Kinetic Properties Of Ca'+-independent mentioning
confidence: 99%
“…In this respect, retinoid-induced cell differentiation has been shown to regulate the expression of phospholipase A2 (82). Several reports have suggested that phospholipase A2 levels are abnormal in the functional psychoses (109)(110)(111). It should also be noted that arachidonic acid is a ligand for the PPARs, which interact as heterodimeric partners with the RXRs to regulate the expression of multiple target genes.…”
Section: Future Directionsmentioning
confidence: 99%