2003
DOI: 10.1016/s0024-3205(03)00561-7
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Altered expression of NCAM in hippocampus and cortex may underlie memory and learning deficits in rats with streptozotocin-induced diabetes mellitus

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Cited by 93 publications
(65 citation statements)
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“…In this study, diabetes mellitus enhanced the time and travelled paths in 3 blocks with respect to the control group, which is in agreement with similar studies of this type such as the learning deficits with severe impairment of Morris water maze performance following 30 days induction of STZ-induced diabetes (16), an increased escape latency and travelled path to find the hidden platform in Morris water maze test, both in 1 week and 12 weeks STZ-induced diabetes (17), the significant reduction of step down inhibitory avoidance test and an increase in acetyl cholinesterase activity after 30 day diabetes induction in rats (18), in addition to compromising cognition and behavioral aspects in two groups of juvenile rats with 10 and 20 days induction of diabetes, although the impairment progressively increased over time (19). The impairment of cognition in STZ-induced diabetic rats, which is seen as an increased escape latency and travelled distance, is in parallel to the high glucose concentration in the diabetic group in the present study.…”
Section: Discussionsupporting
confidence: 92%
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“…In this study, diabetes mellitus enhanced the time and travelled paths in 3 blocks with respect to the control group, which is in agreement with similar studies of this type such as the learning deficits with severe impairment of Morris water maze performance following 30 days induction of STZ-induced diabetes (16), an increased escape latency and travelled path to find the hidden platform in Morris water maze test, both in 1 week and 12 weeks STZ-induced diabetes (17), the significant reduction of step down inhibitory avoidance test and an increase in acetyl cholinesterase activity after 30 day diabetes induction in rats (18), in addition to compromising cognition and behavioral aspects in two groups of juvenile rats with 10 and 20 days induction of diabetes, although the impairment progressively increased over time (19). The impairment of cognition in STZ-induced diabetic rats, which is seen as an increased escape latency and travelled distance, is in parallel to the high glucose concentration in the diabetic group in the present study.…”
Section: Discussionsupporting
confidence: 92%
“…Therefore, it is likely that glucose reduction is the cause of the improved performance. Alterations of glucose metabolism, interactions with Aβ or altered expression of neuronal cell adhesion molecules (NCAMs) are among the potential mechanisms involved in spatial learning and memory deficits in diabetes mellitus (2,16). Amyloid-β accumulation in neurons can impair memory through the Janus kinase and signal transducer and activator of transcription (JAK-STAT) pathway in the hippocampus, and the functional long form of the leptin receptor (ob Rb), which is largely expressed in the hippocampus, is associated with the JAK2-STAT5 pathway (20).…”
Section: Discussionmentioning
confidence: 99%
“…Diabetes causes numerous complications, such as retinopathy, renal failure, cardiovascular disease and autonomic neuropathy [2]. Evidence suggests that diabetes also affects the central nervous system, including the hippocampus, a part of the limbic system, which is associated with cognitive functions [3]. Several studies [4,5] have revealed the tight association of diabetes with cognitive impairment and dementia.…”
Section: Introductionmentioning
confidence: 99%
“…Diabetes is characterized by a hyperglycemia that results from an absolute or relative insulin deficiency and is associated with long term complications affecting the eyes, kidneys, heart and nerves (Baydas et al, 2003). Oxidative stress is defined as imbalance between the generation of reactive oxygen species and antioxidant defense capacity of the body that is closely associated with aging and a number of diseases including cancer, cardiovascular diseases, diabetes and diabetic complications (Atalay et al, 2002).…”
Section: Introductionmentioning
confidence: 99%
“…Recent studies have shown that both types of diabetes can increase oxidative stress in blood and treatment with antioxidants such as vitamin E and flavonoids may be used for decreasing of oxidative stress and diabetic complications (Baydas et al, 2003;Vincent et al, 2004). There is good evidence that tea flavonoids intake have a role in protection against degenerative diseases and long-term intake of tea flavonoids can prevent obesity in high fat diet.…”
Section: Introductionmentioning
confidence: 99%