Neuroprotective Effect of Nicotine - Essay Example

? For therapeutic purposes nicotine and nicotine compounds have been explored assuming that they have beneficial effects on learning and memory. From epidemiological studies we know that smokers have lower incidences of disorders like the AD and PD due to the neuroprotective effect of the smoke from the substances. This does not though support smoking of nicotine especially due to the fact that it normally has some undesirable effects on the body. Nicotine normally activates all the neural nicotinic receptor types including the ones which cause side effects. Therefore by designing novel nicotinic drugs that interact selectively with some types of neuronal nicotinic receptors but not all it is quite possible to hit only those receptors that are relevant to the given disease (Rennard, 2008). The nicotinic acetylcholine receptors have their location in the neuromuscular junction, autonomic ganglia and the central nervous system. The channels of the ions are activated by nicotine with the influx of both sodium ions and calcium ions which is closely followed by depolarization. For the sake of neuroprotection we would discuss the 12 subunits of 8 alphas and 4 betas of the CNS by origin. These receptors are though lost with age mostly 50% of them. Allosteric sensitization of the nicotinic acetylcholine receptors is considered to be a novel treatment strategy of the AD (Eysenck & Eaves, 1980). The Galantamine which is the che approved inhibitor for the treatment of AD is highly efficient in improving the cognitive impairment than the che inhibitors themselves. Preclinical studies of the neuroprotective effects of nicotine give stress to vivo whose effects occur by up regulation of the protective protein (Shopland, 1983). Though smoking is associated with the incident of serious diseases like cancer, it should be realized that there is a change in the perception of how smoking most so that of tobacco on cancer. It should therefore be understood that there is a quite dangerous aspect of tobacco that is the nicotine. The pharmacological definition of tobacco in the nineteenth century is that of the isolation and synthesis of nicotine where the extreme toxicity of nicotine which was also confirmed at the time. The prevailing hypothesis among researchers and scientists is that nicotine helps protect the brain by binding to nicotinic acetylcholine receptors that sit on the end of nerve terminals. This action by nicotine is similar to turning up the volume of a radio signal, causes brain cells to increase the release of neurotransmitters depleted in diseases like Alzheimer's and Parkinson's (Factor, 2002). The current evidence of the neuroprotective effect of nicotine is evidenced in the PD disease. Parkinson's disease, PD is the second most common neurodegenerative disorder affecting a bigger percentage of individuals most so those over the age of 65 years. While effective therapy exists for treating the bradykinesia, rigidity and tremor associated with the disease, the causes of these disorders are still unknown and still remain a dream (Shopland, 1983). There is no treatment available to prevent or slow the progressive neuronal loss in the substantial nigral and associated decreased levels of dopamine in the striatum that underlie the cardinal features of the disease. Both retrospective and prospective epidemiological studies have consistently demonstrated an inverse association between cigarette smoking and PD, leading to theories that smoking in general and nicotine in particular might be neuroprotective (Rennard, 2008). Nicotine has been shown in animals to stimulate the release of dopamine in the striatum, and to preserve nigral neurons and striatal dopamine levels in laboratory and most specifically the animals with lesioned nigrostriatal pathways. Just like tobacco, Coffee and caffeine consumption have also been shown in epidemiological studies to be inversely related to PD risk. Caffeine is an adenosine receptor antagonist that enhances locomotors activity in animal models of Parkinsonism (Rennard, 2008). Theophylline, a related compound that has A(2A) receptor blocking properties, has been shown in one small trial to improve motor function in patients with PD. Recently, potent and highly selective A(2A) receptor antagonists have been developed that have demonstrated improvement in motor function in animal models of parkinsonism. Exciting findings are emerging that demonstrate attenuation of dopaminergic neurotoxicity with caffeine and other adenosine receptor antagonists in human given the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), suggesting that these compounds may be neuroprotective (Factor, 2002). Evidence for the neuroprotective potential of nicotine is compelling, but further work is needed before testing these and related compounds in clinical trials for both individuals at high risk of developing PD and those with early, untreated disease (Mills, 1999). For the people to know how to make healthy health decisions most so with regards to the smoking, the people must get adequately informed about the drug in all manner of respect. They have to know what the contradictory nature of the disease is, what causes the disease and the gravious impacts of the disease (Wagner, 2003). This comes along with the ways in which they could be in the position of preventing the impacts. In this manner the people will have the knowhow that will enable them in the first place avoid the disease and to a large extent reduce it given prevention is always better than cure. It is important to know that smoking is harmful to almost all the organs of the body since they cause a disease and generally reduces the health of smokers. Tobacco smoke is a mix of over 7000 chemicals which are all poison and they cause serious damage when they penetrate deep in the body tissues (Eysenck & Eaves, 1980). The body in return tries to fight the destructive effects of the smoke which reach the lungs so fast, in its efforts to try and curb the disease the body gets weaker and weaker and reaches a point of no return. The poisons in smoke pose a danger right away the smoke is absorbed in your blood. Sudden blood clots, heart attacks, and strokes can be triggered by tobacco smoke as well given its nature of high penetration in the blood and the body tissues. Poisons in tobacco smoke disrupt the way your body heals itself. Even smoking a cigarette now and then is enough to hurt you as constant stress to the body tissues also cause diseases. Sitting in a smoky bar raises your odds of a heart attack as the effect of the smoke is intensely variable and can make one start hurting inwardly (Miller, 2006). To make wise decisions it is also vital for the people to be informed about the contradictory nature of smoking. They would also need to know the mechanisms of the neuroprotective effects of nicotine and the inhibitors which come along. They also need to know of the roles of both alpha 4 & 7 in the process of neuroprotection (Longenbaker, 2011). Neurotoxicity induced by glutamate and other excitatory amino acids has been implicated in various neurodegenerative disorders including hypoxic ischemic events, trauma, and Alzheimer's and Parkinson's diseases. We examined the roles of nicotinic acetylcholine receptors in survival of CNS neurons during excitotoxic events. Nicotine as well as other nicotinic receptor agonists protected cortical neurons against glutamate neurotoxicity via alpha4 and alpha7 at least partly by inhibiting the process of apoptosis in near-pure neuronal cultures obtained from the cerebral cortex of fetal rats. Donepezil, Galantamine and tacrine, therapeutic acetyl cholinesterase inhibitors currently is being used for treatment of Alzheimer's disease also protected neuronal cells from glutamate neurotoxicity (BaI?ttig, 1978). Both the protective effects of nicotine and the AChE inhibitors are in most of the cases antagonized by the inhibitors antagonists. Moreover, nicotine and those inhibitors induced up-regulation of the inhibitors. Inhibitors for a non-receptor-type tyrosine kinase, Fyn, and janus-activated kinase 2, suppress the neuroprotective effect of donepezil and Galantamine. Furthermore, a PI3K inhibitor also suppresses the neuroprotective effect of the acetylcholine inhibitors (Factor, 2002). A path physiological consequence of tobacco usage produces changes in the body which in most of the cases contribute to heart disease cancer and the worst forms of respiratory disease. These disorders are difficult to prevent when smoking and the people have to know that the surest way given that tobacco exposure. Statistics has it that 1 out of 3 smokers gets addicted with nicotine and out of these 1 out of three die of the same disorders and tobacco related disease (Longenbaker, 2011). Among the disorders resulting from tobacco use, addiction is unique because its primary manifestation is behavioral; this has implications for treatment with the understanding that addiction also results due to the path physiological basis hence the need for the understanding of all the diseases that are caused by tobacco smoking. The pathophysiology of nicotine exists in a variety ranging from tolerance development, receptor up regulation, physiological dependence and the reinforcement effects of the same (Jinot & Bayard, 1993). Most tobacco users are aware of the risks, and they frequently attempt to avoid it; however, they usually fail. It seems reasonable to conclude that once nicotine addiction is established, the seemingly irrational behavior of continued tobacco use is no more governed by free choice and rational decision-making. In all the cases, systematic treatment can enhance the individual's prognosis. However, treatments for nicotine addiction are generally more effective and less toxic than treatments for any heart disease and cancer given they are resultant diseases from smoking (BaI?ttig, 1978). References BaI?ttig, K, 1978, Behavioral effects of nicotine.. Karger: Basel. Eysenck, HJ, & Eaves, LJ, 1980, The causes and effects of smoking, Sage Publications: Beverly Hills, Calif. Factor, SA, 2002, Parkinson's disease diagnosis and clinical management. Demos: New York. Jinot, J, & Bayard, SP, 1993, Respiratory health effects of passive smoking: lung cancer and other disorders: the report of the U.S. Environmental Protection Agency.. Washington, D.C.: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health . Longenbaker, SN, 2011, Mader's understanding human anatomy & physiology (7th ed.), McGraw-Hill: New York. Miller, MW, 2006, Brain development: normal processes and the effects of alcohol and nicotine. Oxford University Press: Oxford. Mills, T, 1999, Asthma: causes and mechanisms of an epidemic inflammatory disease, Lewis Publishers: Boca Raton. Rennard, SI, 2008, Clinical management of chronic obstructive lung disease (2nd ed.), Informa Healthcare: New York. Shopland, DR, 1983, The Health consequences of smoking: cardiovascular disease: a report of the Surgeon General. Rockville, Md.: U.S. Dept. of Health and Human Services, Public Health Service, Office on Smoking and Health ; Washington, D.C. : For sale by the Supt. of Docs., U.S. G.P.O.. Wagner, HL, 2003, Nicotine, Philadelphia: Chelsea House Publishers. Read More