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Mor microenvironment and its role in promoting tumor growth. Oncogene. 2008;27(45):5904?2. 52. Zamarron BF, Chen W. Dual roles of immune cells and their factors in cancer development and progression. Int J Biol Sci. 2011;7(5):651?. 53. Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell. 2011;144(5):646?4. 54. Joven J, Guirro M, Marine-Casado R, Rodriguez-Gallego E, Menendez JA.
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Ause mitochondrial dysfunction [16], ATP deficiency [25] and apoptosis. The structural similarities between STZ and nitrosamines, including N-nitrosodiethylamine (NDEA) and N-nitrosodimethylamine (NDMA) [26], together with experimental evidence that high doses of STZ cause cancer while lower doses cause diabetes or AD-type neurodegeneration with cognitive impairment [15,16,22] led us to hypothesiz
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N.edu 1 Department of Pathology (Neuropathology), Rhode Island Hospital, 593 Eddy Street, Providence, RI 02903, USAnoted that the striking increases in AD and PD mortality rates followed sharply increased consumption of processed foods, use of preservatives, and demand for nitrogen-containing fertilizers [4]. A common theme resonating from these unnecessary lifestyle trends is that we have inadver
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D that volatile solvents such as benzene, a main constituent of gasoline fuel, seems to interact with the synthesis and catabolism of catecholamines and serotonin in the brain, which might explain the neurotoxic effects of these solvents [53]. In this regard, deficiencies of serotonin or other monoamine neurotransmitters such as dopamine and norepinephrine are linked with depression [54,55]. In re
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Lusions: Early limited exposure to nitrosamines exacerbates the adverse effects of later chronic high dietary fat intake in promoting T2DM and neurodegeneration. The mechanism involves increased generation of ceramides and probably other toxic lipids in brain.Background The prevalence rates of Alzheimer's Disease (AD), Parkinson's disease (PD), obesity, type 2 diabetes mellitus (T2DM), and metabol
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Lusions: Early limited exposure to nitrosamines exacerbates the adverse effects of later chronic high dietary fat intake in promoting T2DM and neurodegeneration. The mechanism involves increased generation of ceramides and probably other toxic lipids in brain.Background The prevalence rates of Alzheimer's Disease (AD), Parkinson's disease (PD), obesity, type 2 diabetes mellitus (T2DM), and metabol
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Gs of: 1) increased risk for developing mild cognitive impairment (MCI), dementia, or AD in individuals with T2DM [7,27] or obesity/dyslipidemic disorders [28]; 2) progressive brain insulin resistance andinsulin deficiency in AD [29-32]; 3) cognitive impairment in experimental animal models of T2DM and/or obesity [33,34]; 4) AD-type neurodegeneration and cognitive impairment in experimentally indu
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Terbalance the tendency of two other major neurotransmitters in the brain dopamine and noradrenaline to encourage overarousal, fear, anger, tension, aggression, violence, obsessive-compulsive actions, overeating, anxiety and sleep disturbances [60].Page 8 of(page number not for citation purposes)BMC Physiology 2009, 9:http://www.biomedcentral.com/1472-6793/9/ConclusionThe present results revealed