neurodegenerative diseases/никотин

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In vitro evidence supporting the therapeutic role of nicotine against neurodegeneration.

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This review supports the necessity of combining fundamental chemical and biological methods to scrutinize potential causative agents in neurodegeneration. This is supported by recent experimental evidence in relation to the use of nicotine as a potential therapeutic agent, especially when following

[Tobacco smoking related DNA and protein adducts and risk of degenerative diseases].

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Tobacco smoke contains many thousands of chemicals including a plethora of carcinogens. Most chemical carcinogens undergo metabolic activation leading to the formation of electrophilic metabolites. These highly reactive species interact with nucleophilic sites in DNA and cellular proteins. Thus as

Nicotine and neurodegeneration in ageing.

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Impairment in cholinergic systems is a highly consistent finding in human dementia. Among cholinergic markers, marked decreases in nicotine binding have been most consistently observed in the telencephalic regions of demented patients and are thought to contribute to the cognitive deficits

Molecular, histological and behavioral evidences for neuroprotective effects of minocycline against nicotine-induced neurodegeneration and cognition impairment: possible role of CREB-BDNF signaling pathway.

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Neurodegeneration is one of the serious adverse effects of stimulant agents such as nicotine. Minocycline possess established neuroprotective properties. The role of CREB-BDNF signaling pathway in mediating the neuroprotective effects of minocycline against nicotine-induced

Pharmacology of nicotine and its therapeutic use in smoking cessation and neurodegenerative disorders.

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During the last decade, nicotine has been used increasingly as an aid to smoking cessation and has been found to be a safe and efficacious treatment for the symptoms of nicotine withdrawal. This period has also seen significant advances in our understanding of the mechanisms underlying the

Electrochemical investigation into the redox activity of Fe(II)/Fe(III) in the presence of nicotine and possible relations to neurodegenerative diseases.

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The biological relevance of Fe(II)/Fe(III) is becoming evermore apparent, especially in relation to its potential role in the progression of neurodegenerative diseases such as Parkinson's and Alzheimer's disease. The reported relationship between smoking and a reduced incidence of neurodegenerative

Tobacco Smoke Exposure Impairs Brain Insulin/IGF Signaling: Potential Co-Factor Role in Neurodegeneration.

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BACKGROUND Human studies suggest tobacco smoking is a risk factor for cognitive impairment and neurodegeneration, including Alzheimer's disease (AD). However, experimental data linking tobacco smoke exposures to underlying mediators of neurodegeneration, including impairments in brain insulin and

Inhibition of human MAO-A and MAO-B by a compound isolated from flue-cured tobacco leaves and its neuroprotective properties in the MPTP mouse model of neurodegeneration.

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Prompted by the findings that smokers have lowered brain and blood platelet monoamine oxidase-A and -B activities compared to non-smokers and that smokers have a lowered incidence of Parkinson's disease, we have examined the neuroprotective properties of an MAO inhibitor,

Application of nicotine enantiomers, derivatives and analogues in therapy of neurodegenerative disorders.

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This review gives a brief overview over the major aspects of application of the nicotine alkaloid and its close derivatives in the therapy of some neurodegenerative disorders and diseases (e.g. Alzheimer's disease, Parkinson's disease, Tourette's syndrome, schizophrenia etc.). The issues concerning

Histological and behavioral protection by (-)-nicotine against quinolinic acid-induced neurodegeneration in the hippocampus.

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Injections of quinolinic acid (60, 180, and 600 nmol) in the dorsal hippocampus induced significant neurotoxicity that was evident 1 day after the injection. By day 3, pyramidal as well as granular cells were affected even at the lowest dose of quinolinic acid, an effect that persisted up to 20

In vivo nicotine exposure in the zebra finch: a promising innovative animal model to use in neurodegenerative disorders related research.

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Nicotine improves cognitive enhancement and there are indications that neurodegenerative (age-related) cognitive disorders could be treated with nicotine-based drugs. The zebra finch is a well-recognized model to study cognitive functioning; hence this model could be used to study the effects of

Reductions in acetylcholine and nicotine binding in several degenerative diseases.

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Alzheimer's disease, Parkinson's disease, and progressive supranuclear palsy are all characterized by loss of neurons in the basal forebrain cholinergic system and by associated reductions in cortical presynaptic cholinergic markers, such as choline acetyltransferase. In this report, we identify

Tobacco Smoke-Induced Brain White Matter Myelin Dysfunction: Potential Co-Factor Role of Smoking in Neurodegeneration.

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BACKGROUND Meta-analysis studies showed that smokers have increased risk for developing Alzheimer's disease (AD) compared with non-smokers, and neuroimaging studies revealed that smoking damages white matter structural integrity. OBJECTIVE The present study characterizes the effects of side-stream

Increased neurodegeneration during ageing in mice lacking high-affinity nicotine receptors.

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We have examined neuroanatomical, biochemical and endocrine parameters and spatial learning in mice lacking the beta2 subunit of the nicotinic acetylcholine receptor (nAChR) during ageing. Aged beta2(-/-) mutant mice showed region-specific alterations in cortical regions, including neocortical

MRSI and DTI: a multimodal approach for improved detection of white matter abnormalities in alcohol and nicotine dependence.

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Our previous proton magnetic resonance spectroscopic imaging ((1)H MRSI) studies showed that the frontal lobe white matter (WM) in smoking recovering alcoholics (sRA) had lower concentrations of N-acetylaspartate (NAA), a marker for neuron viability, compared to both nonsmoking recovering alcoholics

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