Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0038454 (stroke)
147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Memory impairment, headaches and vertigo are considered as initial appearances of chronic cerebral vascular disorder in patients with arterial hypertension (AH). The complex analysis of complaints, cognitive functioning, emotional state and MRI data was conducted in 60 patients with AH, mean age 58,4+/-7,8 years, without a history of stroke and 30 controls matched for age, sex and education. Impairment of cognitive functioning was assessed by the Psychiatric Status Scale (a short version), the Clock Drawing Test, tests of auditory and verbal memory, attention concentration, speed of test performance, speech fluency and spatial orientation. The deterioration effect of systolic arterial pressure on cognitive functioning was found. The lesions of white matter (subcortical and/or periventricular leucoaraiosis) were observed in 76% of patients and single asymptomatic lacunar infarctions--in 20%. Cerebral vascular lesions were correlated with cognitive impairment. Anxiety and anxiety-depressive disorders which were not associated with the cerebral vascular lesion but related in large to the patient's complaints on headaches and vertigo were revealed in 62% of cases. The results of the study suggest that cognitive dysfunction proves to be the early and reliable predictor of chronic cerebral vascular disorder in patients with arterial hypertension.
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PMID:[Cognitive disturbances in patients with arterial hypertension]. 1845 93

AIT-082 (an analog of hypoxanthine) is an orally-active nerve growth factor (NGF) agonist under development by NeoTherapeutics as a potential treatment for Alzheimer's disease (AD), stroke and motor neuron disease. A phase II safety and efficacy trial in AD, originally scheduled to begin in the summer of 1997 [283677], began in May 1998 [286975,285562]. The study will enroll more than 60 AD patients [286975]. In February 1998, NeoTherapeutics began a phase I multiple-dose pharmacokinetic study of AIT-082 in 24 healthy elderly volunteers. Subjects of the phase I study will be administered AIT-082 once a day for 7 consecutive days at doses of 100 to 2000 mg per dose [279422]. A limited double-blind, placebo-controlled phase I/II trial in 10 AD patients commenced in Canada in the first quarter of 1997. Treatment with 4000 mg improved memory in 60% of the patients within 3 h, as determined by the word recall test. A decrease in memory was observed in 80% of placebo-treated patients [257132]. A phase I US trial, conducted by the Alzheimer's Disease Cooperative Study, with funding from the National Institute of Aging, began in July 1997. AIT-082 was administered to eight healthy, elderly volunteers as part of an escalating single-dose study. Oral administration of AIT-082 was well-tolerated at high doses [284325] AIT-082 also enhanced memory function in both young adult and aged mice within 2 h of oral administration. Prophylactic treatment prevented or delayed the onset of age-induced memory deficits in mice when administered in drinking water. When memory impairment was produced by brain lesions, the drug restored memory performance and increased the genetic expression of neurotrophin-3 (NT-3), a natural protein growth factor associated with nerve cell function [284325]. AIT-082 appears to have at least three effects on the growth of PC-12 cells in culture. Firstly, it stimulates outgrowth of neurites, secondly it potentiates the growth effects of neurotrophin, and thirdly, it stimulates the synthesis of certain neurotrophins (nerve growth factor, neurotrophin-3 and fibroblast growth factor) and pleiotrophins by astrocytes. These progrowth mechanisms are thought to form the basis of the ability of AIT-082 to restore and prevent age-related working memory deficits in mice [195438]. In October 1997, further preclinical results were presented, demonstrating that treatment with AIT-082 produced an increase in neurotrophic factors following spinal cord injury in rats. This study was conducted at NeoTherapeutics and McMaster University, and was partially funded by the Amyotrophic Lateral Sclerosis Society of Canada. After 7 days of treatment, rats with spinal cord injuries showed an increase in the levels of CNTF and BDNF, naturally occurring growth factors in the spinal cord [267514].
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PMID:AIT-082 NeoTherapeutics Inc. 1846 24

Cognitive deficits, including spatial memory impairment, are very common after ischemic stroke. Neurogenesis in the dentate gyrus (DG) contributes to forming spatial memory in the ischemic brain. Fluoxetine, a selective serotonin reuptake inhibitor, can enhance neurogenesis in the hippocampus in physiological situations and some neurological diseases. However, whether it has effects on ischemia-induced spatial cognitive impairment and hippocampal neurogenesis has not been determined. Here we report that fluoxetine treatment (10 mg kg(-1), i.p.) for 4 weeks promoted the survival of newborn cells in the ischemic hippocampus and, consequently, attenuated spatial memory impairment of mice after focal cerebral ischemia. Disrupting hippocampal neurogenesis blocked the beneficial effect of fluoxetine on ischemia-induced spatial cognitive impairment. These results suggest that chronic fluoxetine treatment benefits spatial cognitive function recovery following ischemic insult, and the improved cognitive function is associated with enhanced newborn cell survival in the hippocampus. Our results raise the possibility that fluoxetine can be used as a drug to treat poststroke spatial cognitive deficits.
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PMID:Chronic fluoxetine treatment improves ischemia-induced spatial cognitive deficits through increasing hippocampal neurogenesis after stroke. 1871 44

It is well established that patients with semantic memory impairment show a relative sparing of general superordinate information as compared with more detailed item-specific information. The objective of the current study was to examine whether or not this superordinate superiority effect is also reliably observed in individuals with stroke. The participants were 3 patients with a diagnosis of semantic dementia (SD) and 4 left middle cerebral artery stroke patients. In the first experiment, participants were administered a series of spoken-word-picture matching tasks, in which picture identity was probed under two conditions: item name (e.g., goose, beetle, shark, hedgehog) and superordinate name (e.g., bird, insect, fish, mammal). The SD patients showed the predicted pattern of performance, identifying stimuli significantly more accurately by their superordinate term than by their specific name. By contrast, the stroke patients showed the reverse pattern of inferior performance in the superordinate condition in all versions of the experimental task. In a second experiment comparing comprehension ofbasic-level names (e.g., dog, bird, fish) and subordinate-level names (e.g., Dalmatian, sparrow, trout), stroke patients also showed a reversal of the normal basic-level effect, showing less accurate comprehension of basic-level names. The pattern of results documented among the stroke patients cannot be accommodated obviously or readily by existing models of conceptual knowledge. These contrasting abilities of SD patients, stroke patients, and normal healthy participants to process subordinate, basic-level, and superordinate names are considered in relation to disorders of executive processing and taxonomic categorization.
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PMID:Contrasting patterns of comprehension for superordinate, basic-level, and subordinate names in semantic dementia and aphasic stroke patients. 1908 3

Magnolol, honokiol, and obovatol are well-known bioactive constituents of the bark of Magnolia officinalis and have been used as traditional Chinese medicines for the treatment of neurosis, anxiety, and stroke. We recently isolated novel active compound (named 4-O-methylhonokiol) from the ethanol extract of Magnolia officinalis. The present study aimed to test two different doses of ethanol extracts of Magnolia officinalis (5 and 10 mg/kg/mouse, p.o., 1 week) and 4-O-methylhonokiol (0.75 and 1.5 mg/kg/mouse, p.o., 1 week) administered for 7 days on memory impairment induced by scopolamine (1 mg/kg body weight i.p.) in mice. Memory and learning were evaluated using the Morris water maze and the step-down avoidance test. Both the ethanol extract of Magnolia officinalis and 4-O-methylhonokiol prevented memory impairment induced by scopolamine in a dose-dependent manner. The ethanol extract of Magnolia officinalis and 4-O-methylhonokiol also dose-dependently attenuated the scopolamine-induced increase of acetylcholinesterase (AChE) activity in the cortex and hippocampus of mice, and inhibited AChE activity in vitro with IC(50) (12 nM). This study, therefore, suggests that the ethanol extract of Magnolia officinalis and its major ingredient, 4-O-methylhonokiol, may be useful for the prevention of the development or progression of AD.
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PMID:Protective effect of the ethanol extract of Magnolia officinalis and 4-O-methylhonokiol on scopolamine-induced memory impairment and the inhibition of acetylcholinesterase activity. 1934 77

Semantic processing can break down in qualitatively distinct ways in different neuropsychological populations. Previous studies have shown that patients with multimodal semantic impairments following stroke - referred to as semantic aphasia (SA) - show deficits on a range of conceptual tasks due to a failure of semantic control processes in the context of prefrontal and/or temporoparietal infarction. Although a deficit of semantic control would be expected to impair performance in all modalities in parallel, most previous research in this patient group has focussed primarily on tasks employing words. This study explored the consequences of deregulated semantic cognition for an indisputably non-verbal task-naturalistic object use. Patients with SA performed more poorly than control participants on a range of everyday tasks assessed by the Naturalistic Action Test (NAT, Schwartz, M. F., Buxbaum, L. J., Ferraro, M., Veramonti, T., & Segal, M. (2002). Naturalistic action test. Thames Valley Test Company). Moreover, their scores on this assessment correlated with those obtained on language-based semantic tasks, suggesting that a common deficit could underlie the impairment in both modalities. As previously observed in the verbal domain, performance on the NAT was poorer when control processes were taxed by dual-task situations and the inclusion of semantically related distracting objects. A number of characteristics of the patients' action sequences were specifically indicative of deregulated semantic cognition. Their everyday action sequences were highly fragmented by a tendency to abandon subtasks before their completion and engage, instead, in extended periods of aimless "toying" with objects. The patient group also exhibited recurrent perseverative behaviour. These findings parallel the performance of a recurrent connectionist model of naturalistic action developed by Botvinick and Plaut [Botvinick, M. & Plaut, D. C. (2004). Doing without schema hierarchies: A recurrent connectionist approach to normal and impaired routine sequential action. Psychological Review, 111, 395-429], after the mechanism responsible for controlling action in a temporally sensitive manner was damaged. This study provides converging evidence for a failure of control processes underlying semantic memory impairment in SA, which is reflected not only in patients' performance on language-based tasks, but also in the non-verbal domain of naturalistic object use.
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PMID:Exploring multimodal semantic control impairments in semantic aphasia: evidence from naturalistic object use. 1950 Jun 8

When locally infused, the potent vasoconstrictor, endothelin-1 (ET-1) produces partial ischemic damage in many regions of the brain, including the hippocampus. The hippocampus is known for a high density of glucocorticoid receptors and for the potent actions of stress and corticosterone to modulate function. The current experiment evaluates the effects of stress and corticosterone on the severity of memory impairment and anatomical pathology produced by hippocampal mini-stroke. Rats with ET-1-induced mini-stroke were exposed to mild restraint stress (1 h/day) or oral corticosterone (0.5 mg/kg) for 16 consecutive days. Spatial memory was then tested in the Morris water task (MWT) and the ziggurat task (ZT). The groups ET-1+stress and ET-1+corticosterone performed significantly better in both tasks than the ET-1-only group. This suggests that increasing corticosteroid levels alleviates the hippocampal stroke-induced memory deficits. Hippocampal volumetric assessment also revealed that both the post-stroke stress and corticosteroid treatment significantly decreased the volume of hippocampal damage. The findings support the view that elevated levels of corticosterone may exert neuroprotective effects in the hippocampus following stroke.
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PMID:Stress and corticosterone enhance cognitive recovery from hippocampal stroke in rats. 1960 80

Memory impairments are common after stroke, and the anatomical basis for impairments may be quite variable. To determine the range of stroke-related memory impairment, we identified all case reports and group studies through the Medline database and the Science Citation Index. There is no hypothesis about memory that is unique to stroke, but there are several important facets of memory impairment after stroke: (1) Every node of the limbic system implicated in memory may be damaged by stroke but very rarely in isolation and the combination of amnesia with the associated deficits often illuminates additional aspects of memory functions. (2) Stroke produces amnesia by damage to critical convergence white matter connections of the limbic system, and stroke is the only etiology of amnesia that can delineate the entire pathway of memory and critical convergence points. (3) Stroke also impairs memory, without causing classical amnesia, by damaging brain regions responsible for cognitive processes, some modality specific and some more generally strategic, that are essential for normal learning and recall.
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PMID:Stroke and episodic memory disorders. 1966 37

A model of hemorrhagic stroke (HS) (intracerebral posttraumatic hematoma) has been used to show that oral Actoinvit (substance S-1) in a daily dose of 500 mg/kg for 7 days causes a steady-state antistroke effect. At the same time the major neurological parameters became lower and the total indices of orientative-trying behavior improved 24 hours just after administration of the drug. Muscle tone, coordination of movements, and memory impairment recovered on days 7-14 after the simulation of HS. The course use of the agent prevented death from HS in 80% of the animals.
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PMID:[Antistroke activity of Actoinvit (substance S-1) in experimental hemorrhagic stroke]. 2014 4

Previous studies have demonstrated that the generation of reactive oxygen species and an excessive inflammatory reaction are involved in the progression of neural damage following brain ischemia. In this study, we focused on the anti-inflammatory and antioxidant properties of eicosapentaenoic acid (EPA). Gerbils were treated intraperitoneally with 500 mg/kg of EPA ethyl for 4 weeks until the day of forebrain ischemia, which was induced by occluding the bilateral common carotid artery for 5 minutes. In the first part of the 2-part experiment, the effect of EPA treatment was evaluated using hematoxylin and eosin staining and deoxynucleotidyl transferase-mediated dUTP nick-end labeling as a marker of cell death (n=3 per group). The inflammatory reaction was evaluated using anti-Iba1 immunohistochemistry, a marker of microglial activation (n=3 per group), and detection of 8-hydroxyl-2'-deoxyguanosine, a marker of oxidative DNA damage (n=4 per group). In the second part of the experiment, the effect of EPA treatment on memory function was examined using an 8-arm radial maze (n=6 per group). EPA treatment significantly inhibited DNA oxidative damage (P < .05) and accumulation of Iba1-positive cells in the CA1 area at 12 and 72 hours after the induction of ischemia, and also decreased apoptotic neurons and neuronal death (P < .001) at 72 hours after ischemia. EPA treatment also significantly improved memory function (P < .05). These findings suggest that EPA inhibits the inflammatory reaction and oxidative damage occurring after ischemic brain injury, and also may contribute to the prevention of neural damage and memory impairment following such injury.
J Stroke Cerebrovasc Dis
PMID:Eicosapentaenoic acid prevents memory impairment after ischemia by inhibiting inflammatory response and oxidative damage. 2062 17


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