Halaman 1 dari 318 hasil
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 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
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
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 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
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
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
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,
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
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
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
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
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
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
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