Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dementia is the development of multiple cognitive deficits that includes memory impairment and at least one of the following--Aphasia, apraxia, agnosia or disturbances in executive functioning. The common causes of dementia among the elderly are Alzheimer's disease, vascular dementia, mixed dementia and Lewy body disease. The concept of reversible dementia was introduced in 1980 when a task force sponsored by National Institute of Ageing found 10-12% of dementia cases in older group to have reversible causes such as metabolic-nutritional, drugs, infections, psychiatric disorders etc. In our series of 76 patients in the presenile age group (<65 years), 34.21% (26/76) had a reversible condition underlying the dementia. 43.42% (33/76) had vascular dementia, 13.15% (10/76) had Alzheimer's disease and 9.21% (7/76) had mixed dementia. Hypertension, hyperlipidemia and diabetes mellitus were commoner in the vascular dementia group as compared to the Alzheimer's group. Evaluation of MRI as a tool in diagnosis of dementia showed increased sensitivity of MRI towards detecting lacunes. The potentially reversible dementias comprised infections 14.47% (11/76), metabolic-nutritional 14.47% (11/76) and autoimmune diseases 3.94% (3/76). These were characterized by a subcortical dementia. Four month follow up of MMSE in this group showed significant and sustained improvement in the metabolic nutritional group.
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PMID:Presenile dementia--etiology, clinical profile and treatment response at four month follow up. 1588 51

It is well accepted that diabetes leads to learning and memory impairment in humans and rodents. Because central delta-opioid receptors have important roles in learning processes, we investigated the involvement of delta-opioid receptors in the spatial learning impairment in streptozotocin (STZ)-induced diabetic mice by the Morris water maze test. The escape latencies to the platform were significantly increased in diabetic mice without changes in the ability to swim. The delta1/delta2-opioid receptor antagonist naltrindole (1 mg/kg/day, s.c.) slightly, but not significantly, reduced the escape latencies in diabetic mice. The selective delta1-opioid receptor antagonist 7-benzylidenenaltrexone (0.3 and 1 mg/kg/day, s.c.), but not the selective delta2-opioid receptor antagonist naltriben (0.3 and 1 mg/kg/day, s.c.), significantly reduced the escape latencies in diabetic mice. These antagonists had no effect on the escape latencies in non-diabetic mice. The selective delta1-opioid receptor agonist [D-Pen2, D-Pen5]-enkephalin (10 nmol/mouse/day, i.c.v.) significantly increased the escape latencies in both non-diabetic and diabetic mice. Based on these results, we suggest that the enhanced response to central delta1-opioid receptors in diabetic mice is involved, at least in part, in the spatial learning impairment in the Morris water maze test.
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PMID:Involvement of delta1-opioid receptors in the spatial learning impairment in streptozotocin-induced diabetic mice. 1631 98

Memory impairment induced by intracerebroventricular (ICV) injection of streptozotocin (STZ) in rats is associated with impaired brain glucose and energy metabolism, oxidative stress and impaired cholinergic neurotransmission. Treatment with antioxidants and cholinergic agonists has been reported to produce beneficial effect in this model. However, no reports are available on drugs that improve glucose utilization and metabolism. In the present study, we evaluated the effects of pioglitazone on cognitive performance, oxidative stress and glucose utilization in ICV STZ injected rats (3 mg/kg, on day 1 and 3). Pioglitazone (10 and 30 mg/kg) was administered per oral (p.o.) for 14 days, starting 5 days prior to STZ injection. Cognitive performance was assessed using step-through passive avoidance and Morris water maze task. Malondialdehyde (MDA) and glutathione levels in brain were estimated as parameters of oxidative stress. Glucose utilization by brain was assessed as the amount of glucose consumed from the media by the brain. ICV STZ injected rats showed a severe deficit in learning and memory associated with increased MDA levels (+67.5%), decreased glutathione levels (-29.2%) and impaired cerebral glucose utilization (-44.4%). In contrast pioglitazone treatment improved cognitive performance, lowered oxidative stress and improved cerebral glucose utilization in ICV STZ rats. The present study demonstrates the beneficial effects of pioglitazone in the ICV STZ induced cognitive deficits, which can be exploited for the dementia associated with diabetes and age-related neurodegenerative disorder, where oxidative stress and impaired glucose and energy metabolism are involved.
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PMID:Chronic administration of pioglitazone attenuates intracerebroventricular streptozotocin induced-memory impairment in rats. 1690

The effect of sulfur dioxide (SO(2)) on hippocampus antioxidant status, lipid peroxidation and learning and memory was investigated in diabetic rats. A total of 40 rats were divided into four equal groups: Control (C), SO(2) + C (SO(2)), diabetic (DM) and SO(2) + D (DMSO(2)). Experimental diabetes mellitus (DM) was induced by i.v injection of alloxan with a dose of 50 mg/kg body weight. Ten ppm SO(2) was administered to the rats in the sulfur dioxide groups in an exposure chamber. Exposure occurred 1 h/d, 7 d/wk, for 6 wk; control rats were exposed to filtered air during the same time periods. SO(2) exposure, while markedly increasing Cu-Zn Superoxide dismutase activity, significantly decreased glutathione peroxidase activity in diabetic and non-diabetic groups compared with the C group; hippocampus catalase activity was unaltered. Hippocampus thiobarbituric acid reactive substances (TBARS) were found to be elevated in all experimental groups with respect to control group. The active avoidance training results indicated that diabetic condition has been associated with learning and memory impairment. SO(2) exposure caused deficits of learning and memory. Diabetes mellitus-induced impairment of learning and memory were potentiated by SO(2) exposure. These findings suggest that exposure to SO(2) by increasing lipid peroxidation, can change antioxidant enzyme activities and can elevated intensity of deficits of learning and memory in diabetic rats.
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PMID:Effect of sulfur dioxide on active and passive avoidance in experimental diabetes mellitus: relation to oxidant stress and antioxidant enzymes. 1761 16

Diabetes mellitus is associated with certain neurological problems such as depression, anxiety, memory impairment, etc. As chromium picolinate (CrP), a widely used trace element is shown to have beneficial effects in diabetes and depression, we investigated its effects on elevated plus maze and spontaneous alternation behavior paradigm as a measure of anxiety and memory, respectively. CrP (8 microg/mL in drinking water) significantly increased percentage preference to open arm in elevated plus maze in diabetic and normal rats. However, no significant changes were observed in percentage alternation after CrP chronic treatment. The possible anxiolytic effect of CrP might be related to its effect on serotonergic transmission.
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PMID:Effect of chronic chromium picolinate in animal models of anxiety and memory. 1786 6

A 65-year-old man experienced an embolism at the left dorsolateral prefrontal region of the brain (the inferior frontal gyrus and a part of the middle frontal gyrus). He was a known case of diabetes mellitus and atrial fibrillation. On evaluation his Mini-Mental State Examination (MMSE) score was 26, indicating the absence of dementia. His chief complaint was episodic memory impairment. On the Wechsler Memory Scale-Revised (WMS-R), he had lower scores for general memory, visual memory and verbal memory. In particular, his verbal memory was markedly impaired compared to visual memory. Tests performed to assess working memory, such as evaluation on the WMS-R for attention/concentration in WMS-R and both parts A and B of the trail making test, revealed normal findings; this indicated that the patient had normal working memory. However, he complained of forgettingess of either phone numbers or routes, and this suggested the impairment of working memory in his daily life. In summary, he suffered from either episodic verbal memory or working memory impairment. His executive function test revealed a slight disturbance of set-exchange on the Wisconsin Card Sorting Test-Keio version. Such a case of memory impairment caused by a lesion in the left dorsolateral prefrontal lobe has rarely been reported.
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PMID:[Memory impairment due to circumscribed infarct at the left dorsolateral prefrontal lobe]. 1840 76

Diabetes-induced learning and memory impairment, characterized by impaired cognitive functions and neurochemical and structural abnormalities, involve direct neuronal damage caused by intracellular glucose. The present study was designed to investigate the effect of lycopene, a potent anti-oxidant and anti-inflammatory molecule, on cognitive functions, oxidative stress and inflammation in streptozotocin (STZ)-induced diabetic rats. Cognitive functions were investigated using a spatial version of the Morris water maze test. Acetylcholinesterase activity, a marker of cholinergic dysfunction, was increased by 1.8 fold in the cerebral cortex of diabetic rats. There was about 2 fold and 2.2 fold rise in thiobarbituric acid-reactive substance levels in cerebral cortex and hippocampus of diabetic rats, respectively. Non-protein thiol levels and enzymatic activities of superoxide dismutase and catalase were decreased in both cerebral cortex and hippocampal regions of diabetic rat brain. Total nitric oxide levels in cerebral cortex and hippocampus was increased by 2.4 fold and 2 fold respectively. Serum tumor necrosis factor-alpha, an inflammatory marker, was found to increase by 8 fold in diabetic rats. Chronic treatment with lycopene (1, 2 and 4 mg/kg; p.o.) significantly and dose dependently attenuated cognitive deficit, increased acetylcholinesterase activity, oxidative-nitrosative stress and inflammation in diabetic rats. The results emphasize the involvement of oxidative-nitrosative stress and peripheral inflammation in the development of cognitive impairment in diabetic animals and point towards the therapeutic potential of lycopene in diabetes-induced learning and memory impairment.
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PMID:Lycopene attenuates diabetes-associated cognitive decline in rats. 1858 96

A 76-year-old man was referred to our hospital because of memory impairment. He was diagnosed as having early Alzheimer's disease, in addition to hypertension and type II diabetes mellitus. Nilvadipine (a Ca-channel blocker), telmisartan (an angiotension II receptor blocker), and pioglitazone (an insulin sensitizer) were administered for the control of the hypertension and diabetes. After 6 months of treatment, the scores on verbal fluency (animals and vegetables/60 seconds) and frontal assessment battery of the patient improved despite no significant changes on the Mini-Mental State Examination and Alzheimer's Disease Assessment Scale. Moreover, follow-up examination of SPECT demonstrated an improvement of cerebral perfusion in the frontal and temporoparietal regions. In addition to nilvadipine, a highly lipophilic Ca channel antagonist agent that easily penetrates the central nervous system, PPARgamma agonists, such as pioglitazone and termisartan, may have had favourable effects on cognitive function and cerebral perfusion in this patient.
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PMID:[A patient with early Alzheimer's disease who showed improvement of cognitive function and cerebral perfusion by combined therapy of nilvadipine and PPAR gamma agonists]. 1875 19

Hypoglycaemic coma and brain injury are potential complications of insulin therapy. Hippocampal neurons are particularly vulnerable to hypoglycaemic stress leading to memory impairment. In the present article, we have investigated the dopamine (DA) content, homovanillic acid (HVA)/DA turnover ratio, DA D(1) and DA D(2) receptors in the hippocampus of insulin-induced hypoglycaemic (IIH) and streptozotocin induced diabetic rats where brain functions are impaired. The DA content decreased significantly in hippocampus of diabetic, diabetic +IIH and control +IIH rats compared to control. The HVA/DA turnover ratio also increased significantly in diabetic, diabetic +IIH and control +IIH rats compared to control. Scatchard analysis using [(3)H] DA in the hippocampus showed a significant increase in DA receptors of diabetic, diabetic +IIH and control +IIH rats with decreased affinity. Gene expression studies using Real-time PCR showed an increased expression of DA D(1) and DA D(2) receptors in the hippocampus of hypoglycaemic and diabetic rats. Our results indicate that the dopaminergic system is impaired in the hippocampus of hypoglycaemic and hyperglycaemic rats impairing DA related functions of hippocampus. We observed a prominent dopaminergic functional disturbance in the hypoglycaemic condition than in hyperglycaemia compared to control. This dopaminergic dysfunction in hippocampus during hypoglycaemia and hyperglycaemia is suggested to contribute to cognitive and memory deficits. This will have clinical significance in the treatment of diabetes.
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PMID:Enhanced dopamine D1 and D2 receptor gene expression in the hippocampus of hypoglycaemic and diabetic rats. 1913 28

Type-2 diabetes is an adult onset condition that affects millions of people worldwide. The ensuing hyperglycemia renders multiple organs to various complications and increases the risk of learning and memory impairment. The Goto-Kakizaki (GK) rat developed from normoglycemic Wistar-Kyoto (WKY) rat is a model for type-2 diabetes, with insulin resistance developing around 12 weeks of age. We presently analyzed the neural progenitor proliferation and survival of the newly generated cells in the dentate gyrus (DG) and the subventricular zone (SVZ) of 6 and 18 week-old GK and WKY rats. At 6 weeks of age, both GK and WKY cohorts showed similar blood glucose levels (112+/-14 mg/dL) and similar rates of neural progenitor proliferation. At 18 weeks of age, the GK rats showed significantly increased blood glucose levels (by 92+/-12%; p<0.05) and higher number of proliferating neural progenitor cells compared to WKY rats (by 183+/-16% in SVZ and by 36+/-5% in DG; p<0.05 in both cases). In both the neurogenic areas, 52+/-9% of the newly formed cells survived to 3 weeks in the 18 weeks old WKY rats, but in the GK rats only 16+/-7% of the new cells survived to 3 weeks. When cultured from the DG of the 18 week old rats in the presence of FGF2 and IGF1, the GK cohort yielded significantly lower number of neurospheres than the WKY cohort (by 69+/-7%; p<0.05). These results indicate that hyperglycemic environment induces proliferation of adult neural progenitors, but detrimental to their survival. Impaired neurogenesis might be a promoter of the decreased brain function in type-2 diabetes.
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PMID:Impaired neurogenesis in adult type-2 diabetic rats. 1913 77


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