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Folate deficiency induces neurodegeneration and brain dysfunction in mice lacking uracil DNA glycosylase.
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Folate deficiency and resultant increased homocysteine levels have been linked experimentally and epidemiologically with neurodegenerative conditions like stroke and dementia. Moreover, folate deficiency has been implicated in the pathogenesis of psychiatric disorders, most notably depression. We
Reduced nerve growth factor levels in stress-related brain regions of folate-deficient mice.
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Folate deficiency has been linked to neurodegenerative and stress-related diseases such as stroke, dementia and depression. The role of the neurotrophins nerve growth factor (NGF) and neurotrophin-3 (NT-3) in stress-related disorders and neurodegeneration has garnered increasing attention in recent
Selective nucleoside triphosphate diphosphohydrolase-2 (NTPDase2) inhibitors: nucleotide mimetics derived from uridine-5'-carboxamide.
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Ecto-nucleoside triphosphate diphosphohydrolases (E-NTPDases, subtypes 1, 2, 3, 8 of NTPDases) dephosphorylate nucleoside tri- and diphosphates to the corresponding di- and monophosphates. In the present study we synthesized adenine and uracil nucleotide mimetics, in which the phosphate residues
Base excision repair activities in organotypic hippocampal slice cultures exposed to oxygen and glucose deprivation.
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The capacity for DNA repair is likely to be one of the factors that determine the vulnerability of neurons to ischemic stress and may influence the pathological outcome of stroke. In this report, initiation of base excision repair (BER) was assessed by analysis of enzyme activity and gene expression
[Cerebral ischemic events and anti-cancer therapy].
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Antineoplastic agents have been associated with cerebral hemorrhage, infarction and cerebral venous thrombosis. Infarctions have been reported in association with L-asparaginase, cisplatinium, methotrexate and 5-fluro-uracil. The mechanisms by which antineoplastic agents may lead to stroke include
DNA damage responses in neural cells: Focus on the telomere.
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Postmitotic neurons must survive for the entire life of the organism and be able to respond adaptively to adverse conditions of oxidative and genotoxic stress. Unrepaired DNA damage can trigger apoptosis of neurons which is typically mediated by the ataxia telangiectasia mutated (ATM)-p53 pathway.
Mitochondrial and nuclear DNA-repair capacity of various brain regions in mouse is altered in an age-dependent manner.
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Aging is associated with increased susceptibility to neuronal loss and disruption of cerebral function either as a component of senescence, or as a consequence of neurodegenerative disease or stroke. Here we report differential changes in the repair of oxidative DNA damage in various brain regions
Purinergic signalling: from normal behaviour to pathological brain function.
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Purinergic neurotransmission, involving release of ATP as an efferent neurotransmitter was first proposed in 1972. Later, ATP was recognised as a cotransmitter in peripheral nerves and more recently as a cotransmitter with glutamate, noradrenaline, GABA, acetylcholine and dopamine in the CNS. Both
Folate deficiency increases postischemic brain injury.
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OBJECTIVE
Folate deficiency and resultant hyperhomocysteinemia impair vascular function and increase stroke risk. We tested the hypothesis that folate deficiency and high homocysteine levels promote DNA damage and increase brain injury after cerebral ischemia/reperfusion.
METHODS
129/Sv mice,
The new P2Y-like receptor G protein-coupled receptor 17 mediates acute neuronal injury and late microgliosis after focal cerebral ischemia in rats.
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G protein-coupled receptor 17 (GPR17), the new P2Y-like receptor, is phylogenetically related to the P2Y and cysteinyl leukotriene receptors, and responds to both uracil nucleotides and cysteinyl leukotrienes. GPR17 has been proposed to be a damage sensor in ischemic stroke; however, its role in
Folic acid, neurodegenerative and neuropsychiatric disease.
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Folic acid plays an important role in neuroplasticity and in the maintenance of neuronal integrity. Folate is a co-factor in one-carbon metabolism during which it promotes the regeneration of methionine from homocysteine, a highly reactive sulfur-containing amino acid. Methionine may then be
NMR analysis of the rat neurochemical changes induced by middle cerebral artery occlusion.
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Stroke is a leading cause of death and disability, affecting millions of people worldwide with almost 80% of them as ischemic stroke and understanding the multiple mechanisms underlying cerebral ischemia is essential for development of effective treatments. To understand metabolic changes induced by
Regio- and Stereoselective Steroid Hydroxylation at the C7-Position by Cytochrome P450 Monooxygenase Mutants.
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Steroidal C7β alcohols and their respective esters have shown significant promise as neuroprotective and anti-inflammatory agents to treat chronic neuronal damage like stroke, brain trauma and cerebral ischemia. Since position C7 is spatially far away from any functional groups that could direct C-H
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