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Fects is clearly warranted. In this regard, guidance may be obtained from what is already known about STZ-induced diseases. STZ, like other N-nitroso compounds, causes cellular injury and disease by functioning as: 1) an alkylating agent and potent mutagen [14]; 2) an inducer of DNA adducts leading to increased apoptosis [23]; 3) a mediator of unscheduled DNA synthesis, triggering cell death [14];
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Fects is clearly warranted. In this regard, guidance may be obtained from what is already known about STZ-induced diseases. STZ, like other N-nitroso compounds, causes cellular injury and disease by functioning as: 1) an alkylating agent and potent mutagen [14]; 2) an inducer of DNA adducts leading to increased apoptosis [23]; 3) a mediator of unscheduled DNA synthesis, triggering cell death [14];
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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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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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Urs), rats were sacrificed by i.p. injection of pentobarbital (120 mg/kg). Blood and cerebella were harvested immediately. Blood or serum was used to measure glucose, insulin, cholesterol, triglycerides, and free fatty acid levels, as previously described [45,46]. Cerebella were harvested for histopathological, biochemical, and molecular studies. For histopathology, tissue samples were immersion f
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Ther hand, recent studies showed that HFD feeding causes obesity, T2DM, and cognitive impairment, but is not sufficient to cause AD [45,46]. Therefore, it's likely that chronic HFD feeding which results in peripheral insulin resistance may provide a second-hit, and that combined with low-dose nitrosamine or other environmental exposures, it may increase the severity of neurodegeneration. In the pr
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Agent for RNA extraction and QuantiTect SYBR Green PCR Mix were obtained from Qiagen, Inc (Valencia, CA). The AMV 1st Strand cDNAPostnatal day 3 (P3) Long Evans rat pups (mean body weight 10 g) were given 3 alternate day intra-peritoneal (i.p.) injections of 20 g NDEA or vehicle. Upon weaning, male rats (N = 8-10 per group) were pair-fed for 8 weeks with high fat (HFD) or low fat (LFD) chow diets.
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Urs), rats were sacrificed by i.p. injection of pentobarbital (120 mg/kg). Blood and cerebella were harvested immediately. Blood or serum was used to measure glucose, insulin, cholesterol, triglycerides, and free fatty acid levels, as previously described [45,46]. Cerebella were harvested for histopathological, biochemical, and molecular studies. For histopathology, tissue samples were immersion f