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Phospholipase A(2) activation as a therapeutic approach for cognitive enhancement in early-stage Alzheimer disease. Schaeffer EL, Forlenza OV, Gattaz WF. Psychopharmacology (Berl). 2009 Jan;202(1-3):37-51. Epub 2008 Oct 14. PMID: 18853146 DOI: 10.1007/s00213-008-1351-0

Phospholipase A(2) activation as a therapeutic approach for cognitive enhancement in early-stage Alzheimer disease. Schaeffer EL, Forlenza OV, Gattaz WF. Psychopharmacology (Berl). 2009 Jan;202(1-3):37-51. Epub 2008 Oct 14. PMID: 18853146 DOI: 10.1007/s00213-008-1351-0

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"High blood levels of leptin, a hormone that regulates appetite, may guard against Alzheimer's disease, new research suggests. "Hopefully, in 10 or 15 years this may be one of many agents that we use to reduce the risk of Alzheimer's disease," said senior study author Dr. Sudha Seshadri, an associate professor of neurology at Boston University School of Medicine. "Or it may be one of many markers that we measure in combination to predict risk." But many more studies of different population groups are needed to determine whether leptin can play such a pivotal role in predicting the risk of Alzheimer's, Seshadri said. The research, which was reported in the Dec. 16 issue of the Journal of the American Medical Association, was done because "there has been some data relating body weight to the risk of Alzheimer's disease," Seshadri said. "When we looked at animal studies, we found some data to indicate that leptin not only produces a feeling of satiety but also has a beneficial effect on the hippocampus. It was important to see if that was true in humans." The hippocampus is a portion of the brain that plays a role in important aspects of memory."

Dietary composition modulates brain mass and solubilizable Abeta levels in a mouse model of aggressive Alzheimer's amyloid pathology. Pedrini S, Thomas C, Brautigam H, Schmeidler J, Ho L, Fraser P, Westaway D, Hyslop PS, Martins RN, Buxbaum JD, Pasinetti GM, Dickstein DL, Hof PR, Ehrlich ME, Gandy S. Mol Neurodegener. 2009 Oct 21;4:40. PMID: 19845940 doi:10.1186/1750-1326-4-40 INTERPRETATION: Dissociation of Abeta changes from brain mass changes raises the possibility that diet plays a role not only in modulating amyloidosis but also in modulating neuronal vulnerability. However, in the absence of a study of the effects of a high protein/low carbohydrate diet on nontransgenic mice, one cannot be certain how much, if any, of the loss of brain mass exhibited by high protein/low carbohydrate diet-fed TgCRND8 mice was due to an interaction between cerebral amyloidosis and diet. Given the recent evidence that certain factors favor the maintenance of cognitive function in the face of substantial structural neuropathology, we propose that there might also exist factors that sensitize brain neurons to some forms of neurotoxicity, including, perhaps, amyloid neurotoxicity. Identification of these factors could help reconcile the poor clinicopathological correlation between cognitive status and structural neuropathology, including amyloid pathology.