Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this retrospective study was to determine the prevalence of alcoholism among terminally ill cancer patients when assessed by multidisciplinary interviews and by the CAGE Questionnaire. We reviewed the charts of 100 consecutive patients assessed by a multidisciplinary team for the presence of alcoholism during 1989, and 100 consecutive patients assessed by the CAGE Questionnaire during 1992. Alcoholism was diagnosed in 28/100 patients during 1989 (28%) and 18/66 patients during 1992 (27%). Thirty-four patients were unable to complete the CAGE Questionnaire in 1992 because of sedation or cognitive impairment; six of these patients (17%) were found to be alcoholics after multidisciplinary assessment. Only 9/28 (32%) and 8/24 (33%) patients diagnosed as alcoholics during 1989 and 1992, respectively, had been previously diagnosed as alcoholics according to the medical charts. The mean equivalent daily dose of morphine during admission and on Day 2 during 1992 were 153 +/- 193 mg and 183 +/- 198 for alcoholic patients, versus 58 +/- 80 and 70 +/- 79 mg for nonalcoholics (P = 0.06 and 0.03, respectively). The maximal dose of opioid and the pain intensity during admission, however, were not significantly different between alcoholics and nonalcoholics. Our results suggest that alcoholism is highly prevalent and underdiagnosed among symptomatic terminally ill cancer patients. The CAGE Questionnaire should be used for screening for alcoholism in this population. When multidimensional assessment and management of pain is applied, the outcome of alcoholic patients appears to be similar to that of nonalcoholics.
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PMID:The frequency of alcoholism among patients with pain due to terminal cancer. 859 20

Twenty-two rats were reared in standard conditions during the first two months of their life. Then the animals were divided into two groups exposed to different rearing conditions. Twelve animals (Group SO) were housed socially, six animals per cage, and for three weeks they were subjected to sensory stimulation in an enriched environment. The other ten subjects were kept individually (Group IN); one rat per mesh cage, in conditions of relatively impoverished sensory stimulation. In both groups the training of the conditioned emotional response (CER) was performed when animals were three months old. In contrast to IN subjects, the rats subjected to permanent social contacts and reared in the enriched environment (Group SO) revealed almost equally low instrumental response rates in trials with the conditioned stimulus (CS) paired with nociceptive foot-shock (US), and in periods when no CS and/or US were applied. The results suggested that early exposure to an enriched environment caused a later decrease of the animals' capability to differentiate between the aversive CS and cues of the experimental context. This cognitive impairment was probably a secondary effect of fear generalized to the entire experimental situation.
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PMID:Effects of social rearing conditions on conditioned suppression in rats. 1200 70

The objective of this study was to determine the frequency of cognitive impairment in patients with rheumatoid arthritis (RA). A cross-sectional study of 40 patients with RA and 40 healthy controls was performed. To assess cognitive impairment, anxiety and depression, the following standardized psychiatric and clinical research methods were used: the Mini-Mental State Examination (MMSE), logic memory tests, short and long memory tests, verbal fluency tests, attention tests, the Brief Psychiatric Rating Scale (BPRS), the Hospital Anxiety and Depression (HAD)/CAGE scale and the Beck Depression Inventory (BDI). Patients and controls with incomplete primary education were excluded from the study. Statistics were performed by chi-square test and by Fisher's exact test. Cognitive impairment was observed in 30% of patients with RA and in 7.5% (p < 0.05) of healthy controls. Patients with RA had a significantly worse outcome in verbal fluency (p < 0.05), logic memory (p < 0.05) and short memory (p < 0.05). No statistical difference was observed among the results obtained in the MMSE, BPRS, HAD/CAGE and BDI. There was no significant relation to the duration of the illness, use of corticotherapy or disability. We observed a high prevalence of cognitive impairment in RA patients. Cognitive impairment was not related to clinical and treatment features or disability. More studies are necessary to determine clinical impact of cognitive impairment in RA.
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PMID:Cognitive impairment in rheumatoid arthritis. 1531 12

Cognitive performance is sensitive to both neural and non-neural changes induced by physical activity and inactivity. This study investigated whether access to physical activity outside a standard laboratory animal cage affected cognitive performance as measured by navigation of a spatial maze. It also examined gene expression in heart tissue for genes associated with cardiovascular function given recent reports of cognitive impairment associated with hyperlipidemia. Furthermore, we measured expression of neural-regulatory genes typically expressed in brain, but also found in cardiac tissue. Male Sprague-Dawley rats (n = 72) were separated into three groups having different access to physical activity: none outside a standard cage, twice-weekly physical activity, and every other day exercise on a running wheel. Compared with a sedentary group, spatial maze performance was enhanced in animals that had access to physical activity, either twice-weekly in a large box or every other day on a running wheel. Both the cardiovascular and neural-related genes expressed in the heart were distinguished by access to physical activity. Several genes that are associated with heart rate, cholesterol biosynthesis, blood pressure, and cell adhesion regulation, including GJA1, FDFT1, EDN1, and CD36, differed in animals based on access to physical activity. Neural-related genes expressed in cardiac tissue associated with neurite outgrowth, neuroplasticity, and neurogenesis including RTN4, HOMER2, ACTB, NCDN, KIF5B, and HMGB2, were expressed differently among the three groups. Significant shifts in ten cardiovascular and neural-related gene expressions in cardiac tissue were associated with physical activity and may have influenced learning and performance on a spatial maze.
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PMID:Exercise-induced changes in cardiac gene expression and its relation to spatial maze performance. 1620 79

Homocysteinemia is associated with cognitive dysfunction in the elderly ranging from subtle cognitive decline to dementia. Homocysteine is generated from methionine as a product of biological methylation reactions and is disposed of through reactions that require folate and vitamins B12 and B6. While different disruptions in these reactions can result in homocysteinemia, it is unclear if they will also result in homocysteine-mediated cognitive dysfunction. Young ApoE-deficient mice were fed one of four diets with differing methionine and B-vitamin content for eight weeks, before undergoing psychomotor tests, the Morris Water Maze test of spatial memory and learning, and measurement of home-cage activity. B-vitamin deficiency induced homocysteinemia and selectively impaired Morris Water Maze performance without affecting other behavioral measures. The cognitive deficits occurred in the absence of overt histologic neurodegeneration but in association with moderate impairments of brain methylation potential. Diets that yielded cognitive deficits were different from those that exacerbated aortic pathology. These findings are inconsistent with a single mechanism linking homocysteinemia to neurological dysfunctions mediated by homocysteine vasotoxicity. Instead, they indicate that different "types" of homocysteinemia, or in other words different impairments of nutritional metabolism affecting homocysteine levels, may lead to different end organ dysfunctions and/or diseases.
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PMID:The cognitive impact of nutritional homocysteinemia in apolipoprotein-E deficient mice. 1691 46

Kynurenic acid is an endogenous neuroactive compound whose unbalancing is involved in the pathogenesis and progression of several neurological diseases. Kynurenic acid synthesis in the human brain is sustained by the catalytic activity of two kynurenine aminotransferases, hKAT I and hKAT II. A wealth of pharmacological data highlight hKAT II as a sensible target for the treatment of neuropathological conditions characterized by a kynurenic acid excess, such as schizophrenia and cognitive impairment. We have solved the structure of human KAT II by means of the single-wavelength anomalous dispersion method at 2.3-A resolution. Although closely resembling the classical aminotransferase fold, the hKAT II architecture displays unique features. Structural comparison with a prototypical aspartate aminotransferase reveals a novel antiparallel strand-loop-strand motif that forms an unprecedented intersubunit beta-sheet in the functional hKAT II dimer. Moreover, the N-terminal regions of hKAT II and aspartate aminotransferase appear to have converged to highly similar although 2-fold symmetry-related conformations, which fulfill the same functional role. A detailed structural comparison of hKAT I and hKAT II reveals a larger and more aliphatic character to the active site of hKAT II due to the absence of the aromatic cage involved in ligand binding in hKAT I. The observed structural differences could be exploited for the rational design of highly selective hKAT II inhibitors.
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PMID:Crystal structure of human kynurenine aminotransferase II, a drug target for the treatment of schizophrenia. 1805 96

The endovascular perforation model of subarachnoid hemorrhage (SAH) is a commonly used model in rats as it is performed without a craniotomy and accurately mimics the physiological effects of SAH in humans. The long-term behavioural profile of the model, however, has not been characterized. Given that humans often have cognitive deficits following SAH, we set out to characterize the behavioural profile as well as the spontaneous temperature changes of rats following intraluminal perforation. Rats were pre-trained on three motor tasks (tapered beam, limb-use asymmetry and the horizontal ladder tasks) prior to receiving a SAH. The animals were then assessed on post-surgical days 3, 7, 14 and 21 on these tasks. At the completion of motor testing, the rats were assessed on a moving platform version of the Morris water task. Despite significant mortality (33%), SAH did not result in lasting motor deficits on any of the tasks examined. However, the SAH group did show a minor cognitive impairment in the Morris water task. In addition, SAH produced a slight, but significant elevation in body temperature (vs. sham operated rats) despite an acute decrease in general home cage activity. The majority of the animals did not have any observable infarcts and the SAH did not significantly affect cortical thickness. In summary, the endovascular perforation model of SAH results in no lasting motor deficits and only minor cognitive impairment in survivors, which alone would be difficult to evaluate in neuroprotection or rehabilitation studies.
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PMID:Long-term assessment of motor and cognitive behaviours in the intraluminal perforation model of subarachnoid hemorrhage in rats. 1905 87

Huntington's disease (HD) is an autosomal-dominant neurodegenerative disorder, for which no known cure or effective treatment exists. To facilitate the search for new potential treatments of HD, an automated system for analyzing the behavior of transgenic HD mice is urgently needed. A recently developed behavior screening system, the IntelliCage, allows automated testing of mouse behavior in the home cage employing individual recognition of animals living in social groups. The present study validates the ability of the IntelliCage system to detect behavioral and cognitive dysfunction in R6/2 mice, an established transgenic model of HD. The results indicate that the IntelliCage is a reliable system for recording exploratory activity, drinking behavior, circadian rhythm, spatial preference, and cognition in mice during prolonged periods of assessment. The system detected early dysfunctional behaviors in R6/2 mice, such as decrease in exploratory activity, sleep disturbances, increased drinking, and repetitive behavior. Additionally, the use of various learning tasks, such as spatial avoidance and spatial patrolling, revealed early cognitive changes in R6/2 mice. The simple learning tasks may be used at both early and late stages of the disease.
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PMID:Detection of early behavioral markers of Huntington's disease in R6/2 mice employing an automated social home cage. 1941 Jun 5

Normally, mice sleep during the day and are active at night. In Huntington's disease mice (R6/2 line) this circadian pattern disintegrates progressively over the course of their illness. Cognitive decline and apathy in R6/2 mice can be improved with sleeping drugs, suggesting that sleep disruption contributes to their neurological decline. We wondered if wakefulness was equally important. Here, we used two drugs to manage sleep/wake cycles in R6/2 mice, Alprazolam (to put them to sleep) and Modafinil (to wake them up). We found that both drugs improved cognitive function and apathy, but had a stronger effect when used in combination. Remarkably, beneficial effects on cognitive performance were also seen in vehicle-treated cage-mates of Alprazolam/Modafinil-treated mice, suggesting that behavioral intervention to regularize sleep/wake activity might be therapeutically useful. We suggest that focused management of sleep and wakefulness will slow the progression of cognitive decline and apathy in neurological conditions where sleep is disordered.
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PMID:Management of sleep/wake cycles improves cognitive function in a transgenic mouse model of Huntington's disease. 1945 May 69

Deficits in social behaviour is a characteristic of numerous mental disorders including autism, schizophrenia, depression and Alzheimer's disease. For the assessment of pharmacological and genetic experimental disease models, conventional social interaction tasks bear the uncertainty that any drug-induced abnormality of the investigator may feed back to the drug-free companion modifying its reactions. A considerable technical improvement was recently reported by Moy et al. [Moy SS, Nadler JJ, Perez A, Barbaro RP, Johns JM, Magnuson T, et al. Sociability and preference for social novelty in five inbred strains: an approach to assess autistic-like behaviours in mice. Genes Brain Behav 2004;3:287-302] in which the drug free partner is confined to a small cage and social contacts of the investigator are recorded uncontaminated of any social reactions of the stranger. Using this novel behavioural paradigm, we here show in C57Bl/6 female mice that sociability (social interaction with a stranger mouse) is not impaired after administration of the anxiolytic diazepam (0.1-1 mg/kg) or the muscarinic antagonist scopolamine hydrobromide (0.1-1 mg/kg). However, social memory tested after a short time interval was impaired by both drugs in a dose-dependent manner (diazepam: > or = 0.5mg/kg; scopolamine: > or = 0.3mg/kg). The scopolamine-induced short-term memory deficit was reversed to normal by the choline esterase inhibitor donepezil (1 mg/kg). Given this dependence of social recognition on the cholinergic system, combined with the clinical observation of reduced social contacts in dementia patients, sociability may offer a novel endpoint biomarker with translational value in experimental models of cognitive dysfunction.
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PMID:Scopolamine-induced deficits in social memory in mice: reversal by donepezil. 1952 54


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