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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.

Is Vitamin E Toxic to Neuron Cells?\nThen SM, Mazlan M, Mat Top G, Wan Ngah WZ.\nCell Mol Neurobiol. 2009 Jan 27. [Epub ahead of print]\nPMID: 19172392