Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent advances in molecular biology, biochemistry, cell biology and behavioral pharmacology together with the development of more selective ligands to the various adenosine receptors have increased our understanding of the functioning of central adenosine A(2A) receptors. The A(2A) receptor is one of four adenosine receptors found in the brain. Its expression is highest in striatum, nucleus accumbens and olfactory tubercles, although it also occurs in neurons and microglia in most other brain regions. The receptor has seven transmembrane domains and couples via Gs to adenyl cyclase stimulation. Antagonistic interactions between A(2A) receptors and dopamine D(2) receptors have been described, as stimulation of the A(2A) receptor leads to a reduction in the affinity of D(2) receptors for D(2) receptor agonists. The A(2A) receptor is thought to play a role in a number of physiological responses and pathological conditions. Indeed, A(2A) receptor antagonists may be useful for the treatment of acute and chronic neurodegenerative disorders such as cerebral ischemia or Parkinson's disease. A(2A) receptor agonists may treat certain types of seizures or sleep disorders. This review discusses the characteristics, distribution, pharmacochemical properties and regulation of central A(2A) receptors, as well as A(2A) receptor-mediated behavioural responses and their potential role in various neuropsychiatric disorders.
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PMID:Central adenosine A(2A) receptors: an overview. 1061 96

The premature infant is at increased risk of cerebral white matter injury. Melatonin is neuroprotective in adult models of focal cerebral ischemia and attenuates ibotenate-induced white matter cysts in neonatal mice. Clinically, melatonin has been used to treat sleep disorders in children without major side effects. The aim of this study was to investigate the protective and anti-inflammatory effects of melatonin in the immature brain following intrauterine asphyxia. Fetal sheep at 90 d of gestation were subjected to umbilical cord occlusion. Melatonin (20 mg/kg, n = 9) or vehicle (n = 10) was administered IV to the fetus, starting 10 min after the start of reperfusion and continued for 6 h. Melatonin treatment resulted in a slower recovery of fetal blood pressure following umbilical cord occlusion, but without changes in fetal heart rate, acid base status or mortality. The production of 8-isoprostanes following umbilical cord occlusion was attenuated and there was a reduction in the number of activated microglia cells and TUNEL-positive cells in melatonin treated fetuses, suggesting a protective effect of melatonin. In conclusion, this study shows that melatonin attenuates cell death in the fetal brain in association with a reduced inflammatory response in the blood and the brain following intrauterine asphyxia in mid-gestation fetal sheep.
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PMID:Melatonin reduces inflammation and cell death in white matter in the mid-gestation fetal sheep following umbilical cord occlusion. 1723 14

Carotid artery redundancy with kinking and coiling can be the cause for acute, ischaemic transitory or even permanent, brain damage and cerebrovascular symptoms. The cerebral ischaemia typically associated to kinking of carotid artery is positional and can be provoked by some (extreme) movenets of the head. The awake patient is coscious of those typical head positions, and capable to avoid them. Prolonged uncontrolled turning of the head during sleep has been reported to cause a stroke in sleep or unpleasant phenomena during sleep. The parasomnias and central sleep apnea syndrome caused by ischaemia on the basis of haemodynamically significant reduction of blood flow to the brain bacause of kinking of carotid artery, are not properly analised, investigated, described and classified. Only one case, as far as we know, of obstructive sleep apnea syndrome caused by tortuous internal carotid artery has been published until now. The surgical treatment with resection of proximal redundant segment of internal carotid artery and reimplantation in its anatomical position resolved transient ishaemic attacks and paroxysmal sleep disorders in children. Sleep disorders in patients with kinking of carotid artery could adress the question about the nature of the link between stroke and sleep disorders, which has been found in a significant proportion of patients with paroxysmal cerebral ischaemia caused by kinks and coils. The sleep disorders may be both a risk factor for stroke but also a direct consequence of acute ischaemic transitory or even permanent brain damage. There are some data supporting the hypothesis of a cause-effect relationship between sleeping disorders and brain ischaemia. Comparation between sleep disorders symptoms and signs in patiens with kinking of carotid artery pre and postoperatively (resolved symptoms) could be sutable model for design of investigation of the relationship between brain ischaemia and sleep disorders.
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PMID:[Observation of sleep disorders in patients with kinking of carotid artery]. 2066 20

As an endogenous neuroprotectant agent, adenosine is extensively distributed and is particularly abundant in the central nervous system (CNS). Under physiological conditions, the concentration of adenosine is low intra- and extracellularly, but increases significantly in response to stress. The majority of adenosine functions are receptor-mediated, and primarily include the A1, A2A, A2B, and A3 receptors (A1R, A2AR, A2BR, and A3R). Adenosine is currently widely used in the treatment of diseases of the CNS and the cardiovascular systems, and the mechanisms are related to the disease types, disease locations, and the adenosine receptors distribution in the CNS. For example, the main infarction sites of cerebral ischemia are cortex and striatum, which have high levels of A1 and A2A receptors. Cerebral ischemia is manifested with A1R decrease and A2AR increase, as well as reduction in the A1R-mediated inhibitory processes and enhancement of the A2AR-mediated excitatory process. Adenosine receptor dysfunction is also involved in the pathology of Alzheimer's disease (AD), depression, and epilepsy. Thus, the adenosine receptor balance theory is important for brain disease treatment. The concentration of adenosine can be increased by endogenous or exogenous pathways due to its short half-life and high inactivation properties. Therefore, we will discuss the function of adenosine and its receptors, adenosine formation, and metabolism, and its role for the treatment of CNS diseases (such as cerebral ischemia, AD, depression, Parkinson's disease, epilepsy, and sleep disorders). This article will provide a scientific basis for the development of novel adenosine derivatives through adenosine structure modification, which will lead to experimental applications.
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PMID:Research progress on adenosine in central nervous system diseases. 3133 8