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mice

Acceleration of brain amyloidosis in an Alzheimer's disease mouse model by a folate, vitamin B6 and B12-deficient diet.

Zhuo J-M, Praticò D. Acceleration of brain amyloidosis in an Alzheimer's disease mouse model by a folate, vitamin B6 and B12-deficient diet. Exp Gerontol. 2010;45(3):195-201. doi:10.1016/j.exger.2009.12.005.

Protein phosphatase 2A methyltransferase links homocysteine metabolism with tau and amyloid precursor protein regulation.

Sontag E, Nunbhakdi-Craig V, Sontag J-M, et al. Protein phosphatase 2A methyltransferase links homocysteine metabolism with tau and amyloid precursor protein regulation. J Neurosci. 2007;27(11):2751-9. doi:10.1523/JNEUROSCI.3316-06.2007.

Folate deficiency induces in vitro and mouse brain region-specific downregulation of leucine carboxyl methyltransferase-1 and protein phosphatase 2A B(alpha) subunit expression that correlate with enhanced tau phosphorylation.

Sontag J-M, Nunbhakdi-Craig V, Montgomery L, et al. Folate deficiency induces in vitro and mouse brain region-specific downregulation of leucine carboxyl methyltransferase-1 and protein phosphatase 2A B(alpha) subunit expression that correlate with enhanced tau phosphorylation. J Neurosci. 2008;28(45):11477-87. doi:10.1523/JNEUROSCI.2816-08.2008.

B-vitamin deprivation induces hyperhomocysteinemia and brain S-adenosylhomocysteine, depletes brain S-adenosylmethionine, and enhances PS1 and BACE expression and amyloid-beta deposition in mice.

Fuso A, Nicolia V, Cavallaro RA, et al. B-vitamin deprivation induces hyperhomocysteinemia and brain S-adenosylhomocysteine, depletes brain S-adenosylmethionine, and enhances PS1 and BACE expression and amyloid-beta deposition in mice. Mol Cell Neurosci. 2008;37(4):731-46. doi:10.1016/j.mcn.2007.12.018.

An assessment of lithium using the IEHR Evaluative Process for Assessing Human Developmental and Reproductive Toxicity of Agents. IEHR Expert Scientific Committee.

Moore JA. An assessment of lithium using the IEHR Evaluative Process for Assessing Human Developmental and Reproductive Toxicity of Agents. IEHR Expert Scientific Committee. Reprod Toxicol. 1995;9(2):175-210. Available at: .

Resolvins: a family of bioactive products of omega-3 fatty acid transformation circuits initiated by aspirin treatment that counter proinflammation signals.

Serhan CN, Hong S, Gronert K, et al. Resolvins: a family of bioactive products of omega-3 fatty acid transformation circuits initiated by aspirin treatment that counter proinflammation signals. J Exp Med. 2002;196(8):1025-37. Available at: .

Novel docosanoids inhibit brain ischemia-reperfusion-mediated leukocyte infiltration and pro-inflammatory gene expression.

Marcheselli VL, Hong S, Lukiw WJ, et al. Novel docosanoids inhibit brain ischemia-reperfusion-mediated leukocyte infiltration and pro-inflammatory gene expression. J Biol Chem. 2003;278(44):43807-17. doi:10.1074/jbc.M305841200.

Novel docosatrienes and 17S-resolvins generated from docosahexaenoic acid in murine brain, human blood, and glial cells. Autacoids in anti-inflammation.

Hong S, Gronert K, Devchand PR, Moussignac R-L, Serhan CN. Novel docosatrienes and 17S-resolvins generated from docosahexaenoic acid in murine brain, human blood, and glial cells. Autacoids in anti-inflammation. J Biol Chem. 2003;278(17):14677-87. doi:10.1074/jbc.M300218200.

The role of hippocampal GluR1 and GluR2 receptors in manic-like behavior.

Du J, Creson TK, Wu L-J, et al. The role of hippocampal GluR1 and GluR2 receptors in manic-like behavior. J Neurosci. 2008;28(1):68-79. doi:10.1523/JNEUROSCI.3080-07.2008.

A common mechanism of action for three mood-stabilizing drugs.

Williams RSB, Cheng L, Mudge AW, Harwood AJ. A common mechanism of action for three mood-stabilizing drugs. Nature. 2002;417(6886):292-5. doi:10.1038/417292a.