Effect of Melatonin on Cognitive Ability of Rats and Expression of NCAM in the Brain Structures in Streptozotocin-Induced Diabetes

Nedzvetsky, V. S.; Nerush, P. A.; Кириченко, С. В.

doi:10.1023/b:neph.0000024603.71459.f9

Cited by 6 publications

(5 citation statements)

References 26 publications

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“…Both mRNA and protein expression levels of the ASMT gene affect: auditory-verbal and visual-spatial working memory, verbal fluency, verbal memory, auditory-verbal immediate and deferred memory, the effectiveness of learning, and attention span. These results are in line with the data obtained in studies based on animal models [ 49 ]. Laborie [ 50 ] showed a positive effect of phototherapy and melatonin medication on the improvement of cognitive functioning in 189 patients (mean age 85.8 years) with symptoms of dementia.…”

Section: Discussionsupporting

confidence: 92%

ASMT gene expression correlates with cognitive impairment in patients with recurrent depressive disorder

et al. 2014

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BackgroundRecurrent depressive disorder is a multifactorial disease; one of the typical features is cognitive impairment. The purpose of this study was analysis of ASMT gene expression both on mRNA and protein levels in patients with recurrent depressive disorder (rDD) and assessment of the relationship between plasma level of ASMT protein, gene expression on mRNA level, and cognitive performance.Material/MethodsThe study included 236 subjects: patients with rDD (n=131) and healthy subjects (n=105, CG). Cognitive function assessment was based on: Trail Making Test, The Stroop Test, Verbal Fluency Test (VFT), and Auditory Verbal Learning Test (AVLT).ResultsBoth mRNA and protein expression levels of ASMT gene were significantly higher in healthy subjects when compared to rDD. The average ASMT mRNA expression level measured for the entire group was M=0.21 (SD=0.09), and the protein level was M=12.84 (SD=3.29). In patients with rDD, statistically significant correlations occurred between both mRNA and protein expression levels and part A of the TMT (negative correlation) and verbal fluency test (positive correlation). In the group CG, there was no statistically significant association between the analyzed variables. In the entire group there was a statistically significant correlation between both ASMT mRNA and protein expression levels and all the neuropsychological tests used in the survey.Conclusions1. Our study confirms previous results showing decreased mRNA and protein expression levels of ASMT gene in depression. 2. Our data suggest a relationship between decreased mRNA and protein expression levels of ASMT gene and cognitive impairment.

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Section: Discussionsupporting

confidence: 92%

ASMT gene expression correlates with cognitive impairment in patients with recurrent depressive disorder

et al. 2014

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“…Reduced ASMT gene expression in rDD patients is therefore related to suboptimal functioning in the frontal lobes and hippocampus, areas that underpin working memory, attention and verbal fluency. These results are in line with the data obtained in animal models [ 55 ].…”

Section: Physiological Underpinnings Of Cognitive Dysfunctions In Rddsupporting

confidence: 92%

Mechanisms Underlying Neurocognitive Dysfunctions in Recurrent Major Depression

Gałecki

Talarowska

Anderson³

et al. 2015

Med Sci Monit

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Recent work shows that depression is intimately associated with changes in cognitive functioning, including memory, attention, verbal fluency, and other aspects of higher-order cognitive processing. Changes in cognitive functioning are more likely to occur when depressive episodes are recurrent and to abate to some degree during periods of remission. However, with accumulating frequency and duration of depressive episodes, cognitive deficits can become enduring, being evident even when mood improves. Such changes in cognitive functioning give depression links to mild cognitive impairment and thereby with neurodegenerative conditions, including Alzheimer’s disease, Parkinson’s disease, schizophrenia, and multiple sclerosis. Depression may then be conceptualized on a dimension of depression – mild cognitive impairment – dementia. The biological underpinnings of depression have substantial overlaps with those of neurodegenerative conditions, including reduced neurogenesis, increased apoptosis, reactive oxygen species, tryptophan catabolites, autoimmunity, and immune-inflammatory processes, as well as decreased antioxidant defenses. These evolving changes over the course of depressive episodes drive the association of depression with neurodegenerative conditions. As such, the changes in cognitive functioning in depression have important consequences for the treatment of depression and in reconceptualizing the role of depression in wider neuroprogressive conditions. Here we review the data on changes in cognitive functioning in recurrent major depression and their association with other central conditions.

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“…The present study examined the effects of cinnamic acid treatment on memory impairment, oxidative stress, and cholinergic dysfunction in STZ-induced model of diabetes in mice. Previous studies have suggested that diabetes mellitus is connected with neurological difficulties in the central nervous system [ 38 39 40 ] such as weak learning and memory [ 41 42 43 ]. Based on the concentration, STZ can contribute to type 1 and type 2 diabetes.…”

Section: Discussionmentioning

confidence: 99%

Effects of cinnamic acid on memory deficits and brain oxidative stress in streptozotocin-induced diabetic mice

Hemmati

Alboghobeish

Ahangarpour

2018

Korean J Physiol Pharmacol

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The present study aimed to evaluate the cinnamic acid effect on memory impairment, oxidative stress, and cholinergic dysfunction in streptozotocin (STZ)-induced diabetic model in mice. In this experimental study, 48 male Naval Medical Research Institute (NMRI) mice (30–35 g) were chosen and were randomly divided into six groups: control, cinnamic acid (20 mg/kg day, i.p. ), diabetic, and cinnamic acid-treated diabetic (10, 20 and 40 mg/kg day, i.p. ). Memory was impaired by administering an intraperitoneal STZ injection of 50 mg/kg. Cinnamic acid was injected for 40 days starting from the 21st day after confirming STZ-induced dementia to observe its therapeutic effect. Memory function was assessed using cross-arm maze, morris water maze and passive avoidance test. After the administration, biochemical parameters of oxidative stress and cholinergic function were estimated in the brain. Present data indicated that inducing STZ caused significant memory impairment, whereas administration of cinnamic acid caused significant and dose-dependent memory improvement. Assessment of brain homogenates indicated cholinergic dysfunction, increase in lipid peroxidation and reactive oxygen species (ROS) levels, and decrease in glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) activities in the diabetic group compared to the control animals, whereas cinnamic acid administration ameliorated these indices in the diabetic mice. The present study demonstrated that cinnamic acid improves memory by reducing the oxidative stress and cholinergic dysfunction in the brain of diabetic mice.

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Effect of Melatonin on Cognitive Ability of Rats and Expression of NCAM in the Brain Structures in Streptozotocin-Induced Diabetes

Cited by 6 publications

References 26 publications

ASMT gene expression correlates with cognitive impairment in patients with recurrent depressive disorder

ASMT gene expression correlates with cognitive impairment in patients with recurrent depressive disorder

Mechanisms Underlying Neurocognitive Dysfunctions in Recurrent Major Depression

Effects of cinnamic acid on memory deficits and brain oxidative stress in streptozotocin-induced diabetic mice

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