2012
DOI: 10.1016/j.brainres.2012.06.011
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Possible link between the cognitive dysfunction associated with diabetes mellitus and the neurotoxicity of methylglyoxal

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Cited by 44 publications
(32 citation statements)
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“…We found in this study that hippocampal Bcl-2 and Bcl-XL expressions decreased more and Bax expressions were increasedmore in the hippocampus of diabetic rats than those of the controls. These results are in line with those of many similar studies, most of which were done in vitro Fu et al, 2012;Bournival et al, 2012;Huang et al, 2012). In one of these in vitro studies, Fu et al (2012) reported increased Bax expressions and decreased Bcl-2 expressions in different glucose…”
Section: Accepted Manuscriptsupporting
confidence: 95%
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“…We found in this study that hippocampal Bcl-2 and Bcl-XL expressions decreased more and Bax expressions were increasedmore in the hippocampus of diabetic rats than those of the controls. These results are in line with those of many similar studies, most of which were done in vitro Fu et al, 2012;Bournival et al, 2012;Huang et al, 2012). In one of these in vitro studies, Fu et al (2012) reported increased Bax expressions and decreased Bcl-2 expressions in different glucose…”
Section: Accepted Manuscriptsupporting
confidence: 95%
“…In recent studies, the number of TUNEL positive cells have been observed to increase more in the brains of diabetic animals than in those of the controls (Huang et al, 2012;Liu et al, 2013); but this increase failed to reach statistical significance in the study by Hernández-Fonseca et al (2009). We found in our study that there was significantly more neuronal apoptosis in the hippocampus of diabetic rats than in those of the controls.…”
Section: Accepted Manuscriptcontrasting
confidence: 78%
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“…Also, a number of cellular metabolic pathways about AG neuroprotective functions relate to methylglyoxal (MG) inhibition (40). MG acts as either an endogenous fatal substance (41) or an effective source of ROS (42), which frequently build up in the hippocampal neurons in hyperglycemia (43,44,45). However, the lack of MG, AGEs, ROS and iNOS measurement is a limitation in our study.…”
Section: Discussionmentioning
confidence: 96%
“…In the memory defect due to diabetes, apoptosis in hippocampal neurons plays a primary role (47,48). On the other hand, it has been indicated that apoptosis in the hippocampus due to altering expression of Bcl-2 family proteins in the neurons could relate to reactive MG, ROS and RNS (44,47,49,50). The imbalance of pro/anti-apoptotic signals of Bcl-2 family plays a crucial role in the release of apoptogenic mitochondrial mediators (51,52).…”
Section: Discussionmentioning
confidence: 99%