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Cotinine: a potential new therapeutic agent against Alzheimer's disease.¡¡¥³¥Á¥Ë¥ó¡Ê¥Ë¥³¥Á¥ó¤ÎÀ¸À®Êª¡Ë¡§¥¢¥ë¥Ä¥Ï¥¤¥Þ¡¼É¤ËÂФ¹¤ëÀøºßŪ¤Ê¿·¤·¤¤¼£ÎÅÌô¡£CNS Neurosci Ther¡£ 2012 Jul; 18
ÊÆ¹ñ¹ñΩ°å³Ø¿Þ½ñ´Û National Institutes of Health
Author information¡¡Echeverria V1, Zeitlin R.
Abstract
Tobacco smoking has been correlated with a lower incidence of Alzheimer's disease (AD). This negative correlation has been attributed to nicotine's properties.
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In this review, we discuss evidence showing that cotinine, the main metabolite of nicotine, has many of the beneficial effects but none of the negative side-effects of its precursor.
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Cotinine has been shown to be neuroprotective, to improve memory in primates as well as to prevent memory loss, and to lower amyloid-beta (A¦Â)) burden in AD mice.
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In AD, cotinine's positive effect on memory is associated with the inhibition of A¦Â aggregation, the stimulation of pro-survival factors such as Akt, and the inhibition of pro-apoptotic factors such as glycogen synthase kinase 3 beta (GSK3¦Â).
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Because stimulation of the ¦Á7 nicotinic acetylcholine receptors (¦Á7nAChRs) positively modulates these factors and memory, the involvement of these receptors in cotinine's effects are discussed.
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Because of its beneficial effects on brain function, good safety profile, and nonaddictive properties, cotinine may represent a new therapeutic agent against AD.
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Beneficial effects of nicotine, cotinine and its metabolites as potential agents for Parkinson's disease
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George E. Barreto
Parkinson's disease (PD) is a progressive neurodegenerative disorder, which is characterized by neuroinflammation, dopaminergic neuronal cell death and motor dysfunction, and for which there are no proven effective treatments.The negative correlation between tobacco consumption and PD suggests that tobacco-derived compounds can be beneficial against PD.Nicotine, the more studied alkaloid derived from tobacco, is considered to be responsible for the beneficial behavioral and neurological effects of tobacco use in PD.¡ÊÃæÎ¬¡ËCurrent evidence shows that nicotine, and some of its derivatives diminish oxidative stress and neuroinflammation in the brain and improve synaptic plasticity and neuronal survival of dopaminergic neurons.In vivo these effects resulted in improvements in mood, motor skills and memory in subjects suffering from PD pathology.In this review, we discuss the potential benefits of nicotine and its derivatives for treating PD.
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Introduction
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Parkinson's disease (PD) is the second most common neurodegenerative illness after Alzheimer's disease (AD), and reaches a prevalence of 3% after 65 years of age .Parkinson's disease is characterized by the presence of Lewy bodies, mainly composed of alpha-synuclein fibrils, a depletion of dopamine (DA)-generating neurons in substantia nigra pars compacta (SNc) and ventral tegmental area (VTA) regions of the brain , that results in a decrease of DA levels in the striatum and frontal cortex regions of the brain (Thompson et al., 2005 The cause of death of dopaminergic neurons is still a mystery;however, actual evidence is consistent with the idea that oxidative stress, mitochondrial dysfunction and neuroinflammation are the main factors involved in the etiology of PD ¡¡It has been proposed that various genetic and environmental factors causing mitochondrial dysfunction result in abnormal accumulation of miscoded proteins and the generation of oxidative stress in the brain of subjects with PD
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Nicotine and its derivatives as therapeutic agents against Parkinson's disease
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In spite of over almost 200 years passed from its discovery, there are no drugs available to slow down or stop the progression of PD (Connolly and Lang, 2014 ).Motor symptoms in PD can be improved by N-methyl-NMDA blockers as well as using dopaminergic and anticholinergic compounds.However, the cognitive deficits are not substantially improved by the current therapeutic interventions (Lorenz et al., 2014 ).Furthermore, the most used anti-PD drug, levodopa, produces severe toxic effects such as restlessness, mental impairment, mood changes, and after prolonged use (3–5 years), dyskinesia (Simuni and Sethi, 2008 ).For this reason, the development of potential new therapeutic approaches is imperative¡ÊÃæÎ¬¡Ë.
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Nicotinic acetylcholine receptors regulate synaptic transmission and synaptic plasticity, in several regions of the brain including the midbrain DA centers.These receptors are ligand-gated Ca 2+ , Na + and K + channels, whose activation causes membrane depolarization and the increase of both intraneuronal calcium levels and neurotransmitter release probability.At the postsynaptic sites the activation of the nAChRs also stimulates cell signaling pathways promoting the expression of synaptic proteins mediating, at cellular level, higher cognitive functions such as attention, learning and memory and other cognitive functions (McKay et al., 2007 ).Furthermore, it has been shown that nAChRs activation prevents neurodegeneration by mechanisms involving the activation of pro-survival signaling factors such as phosphatidylinositol 3-kinase (PI3K), Akt and Bcl proteins in the brain (Kawamata and Shimohama, 2011 ).¡ÊÃæÎ¬¡ËAcetylcholine by stimulating the ¦Á7nAChR inhibits the activity of the pro-inflammatory neurothrophic factor kappa B (NF¦ÊB) in human macrophages and consequently the expression and release of cytokines such as the tumor necrosis factor (TNF) by these immune cells (Balakumar and Kaur, 2009 ).¡ÊÃæÎ¬¡Ë
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Several epidemiological studies have shown that tobacco users have a lower incidence or severity of PD (Baron, 1996 ).A meta-analysis of four cohorts and 44 single-subject studies, showed a 40% decrease of risk of developing PD for smokers when compared to never smokers (Hernán et al., 2002 ).Together with smoking, other natural products such as caffeine have shown to be preventative against PD.In one of these studies (Hernán et al., 2002 ), the epidemiological evidence on the association between cigarette smoking, coffee drinking, and the odds of developing PD was reviewed.Results for smoking were calculated based on 44 case-control and four cohort studies, and for coffee on eight case-control and five cohort studies.Compared with never smokers, the relative risk of PD was 0.59 for ever smokers, 0.80 for past smokers, and 0.39 for current smokers.Compared with non-exposed to caffeine controls, relative risk of PD was 0.69 for coffee drinkers.This meta-analysis showed strong epidemiological evidence supporting that in addition to nicotine also caffeine decreased the risk of PD (Chen et al., 2010 ).These findings have been confirmed by several large prospective studies for either coffee or cigarette consumption.Interestingly, other caffeine-containing beverages, such as black tea and Japanese and Chinese teas also reduced PD risk.¡ÊÃæÎ¬¡ËA case-control study assessed the relationship between the ability to quit smoking and nicotine substitute use, in 1808 patients with PD and 1876 sex and age matched controls (Ritz et al., 2014 ).Data from this study revealed that PD patients quit smoking more easily than controls.The authors suggested that this finding was the result of a decreased sensitivity to nicotine in PD patients.Furthermore, they proposed that superior ability to quit smoking is an early sign of PD, similar to constipation, olfactory dysfunction, and sleep disorders.They also suggested that the positive effect of smoking revealed by epidemiologic studies was the result of reverse causation and not a protective effect of nicotine per se .Albeit an interesting observation, newly published evidence, in agreement with previous studies, strongly supports the view that smoking was neuroprotective against PD.The analysis of longitudinal data from 305,468 participants of the NIH-AARP Diet and Health cohort, of whom 1662 had a PD diagnosis, clearly showed that the number of cigarettes and years of smoking inversely and significantly correlated with diminished odds of developing PD.Compared with non-smokers, the odds ratios were 0.78 for past smokers and 0.56 for current smokers.Furthermore, the time of smoking was linked to a lower risk of developing PD.When compared with non-smokers, the odds ratio among past smokers decreased with the smoking duration.Thus, the odds ratio for those who smoked more than 20 cigarettes per day per 1–9, 10–19, 20–29 and 30 years were 0.96, 0.78, 0.64 and 0.59, respectively.These studies strongly suggest that caffeine and nicotine are neuroprotective.
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About the mechanism of neuroprotection, in addition to the mechanisms discussed, a new hypothesis proposes that both cigarette and coffee exert their effects by a completely different mechanism.The hypothesis states that tobacco and caffeine both exert their effects by changing the composition of the microbiota in the gut and consequently reducing intestinal inflammation since pro-inflammatory cytokines are also produced by enteric glial cells (EGC) in the gut (Derkinderen et al., 2014 ).According to this hypothesis, inflammation would promote ¦Á-synuclein aggregation within enteric neurons (EN).The aggregated protein thus may spread to the central nervous system via the vagal preganglionic innervation of the gut and the dorsal motor nucleus of the vagus (DMNV)After several years, the LC and the SN will become affected.Thus, the decrease of inflammation induced by nicotine and caffeine will decrease ¦Á-synuclein aggregation in enteric nerves, and its propagation to the brain.This effect will reduce neurodegeneration and reduce the risk of PD.
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The neuroprotective effect derived from a general reduction of systemic inflammation is an interesting idea that merit further investigation.Certainly, we consider reasonable to propose that the anti-inflammatory effects of nicotine and nicotine-derived compounds is a key contributor to their neuroprotective effects in the brain.The neuroprotective effect of tobacco has been mainly attributed to nicotine, a naturally occurring alkaloid from tobacco that consistently showed beneficial pro-cognitive effects in cellular and animal models of PD (Parain et al., 2003 ).The positive effect of nicotine on motor coordination and behavior has been attributed to its ability to increase DA availability and reduce the production of reactive oxygen species.Although, the detailed mechanism of neuroprotection is not well understood, the activation of nAChRs is considered the main mechanism of action of nicotine against PD (Budzianowski, 2013 ).¡ÊÃæÎ¬¡ËThese results are coherent with the idea that nicotine may prevent PD by stimulating the expression of neuroprotective signaling factors in the brain.
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Acetylcholine Receptors
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Two Types of Receptors
There are two types of acetylcholine receptors (AChR) that bind acetylcholine and transmit its signal:
muscarinic AChRs and nicotinic AChRs, which are named after the agonists muscarine and nicotine, respectively.
These receptors are functionally different, the muscarinic type being G-protein coupled receptors (GPCRs) that mediate a slow metabolic response via second messenger cascades, while the nicotinic type are ligand-gated ion channels that mediate a fast synaptic transmission of the neurotransmitter.
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Nicotine, the Wonder Drug?
This notorious stimulant may enhance learning and help treat Parkinson's, schizophrenia and other neurological diseases.
Wednesday, February 05, 2014
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Called ¡Èthe shaking palsy¡É in an 1817 essay by the English physician James Parkinson (after whom the disease was later renamed), Parkinson's is marked by shaking and difficulty with walking, coordination and all other movements.¡¡Although its ultimate cause remains unexplained, neuroscientists have long known that as symptoms worsen, dopamine-producing neurons in the striatum die out.
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Since the 1960s, the gold-standard treatment for the disease has been the drug levodopa, also known as L-dopa, a dopamine precursor that can cross the blood-brain barrier.¡¡But the drug is not perfect: L-dopa treatment eventually induces dyskinesia — quick, involuntary movements of the hands, and sometimes of the head and trunk.
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Putting together the emerging lines of evidence, Quik decided to treat Parkinson's disease in squirrel monkeys by administering nicotine.¡¡In a landmark 2007 paper, she reported that the monkeys had 50 percent fewer tremors and tics, and that nicotine had reduced dyskinesia 35 percent in those already receiving L-dopa.
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Studies by Quik and others involving rats, mice and nonhuman primates have since found similar effects.¡¡In short, by driving dopamine, nicotine appeared to ease the tremors and tics caused by Parkinson's, and even the movement disorder induced by the major Parkinson's drug.
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Waiting for Human Evidence
Given the findings, one might reasonably ask how many clinical trials of ordinary over-the-counter nicotine patches or gum as a preventative for the progression of Parkinson's have been published in the medical literature.
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Effects of transdermal nicotine on attention and memory in healthy elderly non-smokers .
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Abstract:
Rationale: Nicotine has been found to improve cognitive functions in patients with Alzheimer's disease, but little is known about its effects in the healthy non-smoking elderly. Objectives: This study aimed to investigate the effects of nicotine on cognitive function in healthy non-smoking or nicotine-naïve elderly subjects. Methods: A transdermal patch containing either 5 mg nicotine or placebo was applied on the back of 63 healthy nicotine-naïve or non-smoking elderly Koreans. Cognitive functions were evaluated with the Short Blessed Test, Rey-Kim Memory Test, and digit span test of the Korean-WAIS, both before and 5.5 h after nicotine administration. The plasma level of nicotine after testing was measured using gas chromatography. Results: The subjects' memory functions in trial 5 of the Rey-Kim Memory Tests improved significantly. Furthermore, the effect on memory slope was significantly correlated with the higher plasma level of nicotine. However, the other tests did not reveal any correlation to a significant degree. Conclusions: These results suggest that nicotine of lower plasma level can improve short-term verbal memory functions in non-smoking or nicotine-naïve healthy elderly people and that some effects are dependent on nicotine plasma levels.
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Test uncovers signs of Alzheimer's disease 18 years before diagnosis
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A study of over 2000 people published in Neurology has shown that a test of memory and thinking can reveal differences in people who would go on to develop Alzheimer's disease up to 18 years before diagnosis.¡¡This suggests that the preclinical phase of Alzheimer's disease may begin many years earlier than expected.
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One in three people born in 2015 will develop dementia, new analysis shows¡¡2015ǯ¤ËÀ¸¤Þ¤ì¤Î£³¿Í¤Ë£±¿Í¤¬Ç§Ãξɤòȯ¾É¤¹¤ë
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The research was commissioned by Alzheimer¡Çs Research UK and carried out by the Office of Health Economics.
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¸¦µæ¤Ï±Ñ¹ñ¥¢¥ë¥Ä¥Ï¥¤¥Þ¡¼É¸¦µæ½ê¡ÊAlzheimer Research UK¡Ë¤Ë¤è¤Ã¤Æ°ÑÂ÷¤µ¤ì¡¢ÊÝ·ò°åÎŶɡÊOffice of Health Economics¡Ë¤Ë¤è¤Ã¤Æ¼Â»Ü¤µ¤ì¤¿¡£ It set out to calculate the number of people born today who could be expected to develop the condition during their lifetime. The analysis took into account life expectancy estimates for people born in 2015, as well as estimates of dementia incidence in men and women of different ages. It estimates that:
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32% of people born in the UK in 2015, or one in three, will develop dementia during their lifetime
27% of males born in 2015 will develop the condition
37% of females born in 2015 will develop the condition
George McNamara, Head of Policy at Alzheimer's Society, said:
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Alzheimer's appears to have a worse effect on women than men, review suggests
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Women with memory problems show faster rates of cognitive decline than men
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Ease of Quitting Smoking May Be Early Sign of Parkinson's
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People who are able to quit smoking easily on the first try are significantly more likely to develop Parkinson's disease (PD) than their counterparts who struggle to quit, a new study suggest.The finding, from a large population-based Danish case-control study, supports the notion that patients with PD are able to quit smoking more easily because they have fewer nicotinic receptors in their brain.
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After all, a toothless person has almost certainly suffered from greater tooth decay than someone with teeth, and, therefore, has probably been exposed to more amalgam mercury for a substantial period of time than someone who remains dentate.
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Because mercury stays in the brain for decades, one could be edentulous for a very long time and still have more brain mercury than someone who is dentate and has a lot of amalgams.
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Like Parkinson's and other adult-onset diseases of the central nervous system that now afflict humanity, AD was rare or nonexistent prior to the onset of the Industrial Revolution.
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The Industrial Revolution, which greatly increased human exposure to mercury in the work place and in the environment, got underway in the mid-1700s.
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Amalgam was invented in Europe around 1820 and was widely used throughout Europe and North America by 1850. Parkinson's, MS, and ALS were first mentioned in medical journals in the 1800s.
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It was not until 1906 that German psychiatrist Alois Alzheimer announced that he had found a "strange disease of the cerebral cortex" in the course of performing an autopsy on a demented 56-year-old woman.
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The woman's brain contained an unusual number of the plaques and tangles now considered to be the defining symptoms of AD.
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Scholars affiliated with the University of Minnesota and the Minnesota Pollution Control Agency have demonstrated that atmospheric mercury levels rose dramatically during the 1800's.
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In a 1992 article published in Science, they reported that the rate at which mercury accumulated in seven lakes "increased by a factor of 3 to 4 during the past 140 years."
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Data for six of the seven lakes indicated a substantial increase in deposition rates around 1850 and another increase around 1920. Subsequent research indicates mercury deposition rates may have peaked in the 1970s.
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¡Ú¹õ¿Í¤ÈÇò¿ÍÈæ³Ó¡§Ãî»õ¤¬Â¿¤¤Çò¿Í¤Û¤ÉAD¡Ê¥¢¥ë¥Ä¥Ï¥¤¥Þ¡¼É¡ˤǻà¤Ì¡Û Blacks have far fewer amalgams in their heads than whites;
they also die far less frequently from AD and MS ¹õ¿Í¤ÏÇò¿Í¤è¤ê¤âǾ¤ÎÃæ¤Î¥¢¥Þ¥ë¥¬¥à¡Ê¿å¶ä¹ç¶â¡Ë¤ÏÍÚ¤«¤Ë¾¯¤Ê¤¤¡£
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According to a 1996 report from the Centers for Disease Control, white people are nearly two times more likely to die from AD than blacks.
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According to a 1978 study of MS, "The . . . US Army suggests that the risk of MS for white males is 2.5 times the risk for black males."
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Blacks in the US and England have long had much lower rates of caries than whites.
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Evidence supports the claim that estrogen supplements reduce the risk of AD in women.
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Higher education levels may also protect against AD.
¹âÅù¶µ°é¥ì¥Ù¥ë¤â¤Þ¤¿¡¢AD¤«¤éÊݸ¤ë¤³¤È¤¬¤Ç¤¤ë¡£ Like estrogen, education (or perhaps the habits of mind that higher education encourages) may help the brain maintain or construct neurons.
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¡¡¡¡¡¡¡¡¡¡¡¡¡¡¡ù
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These findings are consistent with the mercury hypothesis.
¤³¤ì¤é¤ÎÃθ«¤Ï¡¢AD¤Î¿å¶äÈȿͲ¾Àâ¤Ç¾§¤¨¤Æ¤¤¤ëÆâÍÆ¤È°ìÃפ¹¤ë¡£ ¡¡¡¡¡¡¡¡¡¡¡¡¡¡¡¡¡þ Trauma to the head is occasionally mentioned in the literature as a factor associated with a higher incidence of AD.
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At least one expert believes head trauma is a risk only for people with the apoE4 gene.
¾¯¤Ê¤¯¤È¤â¡¢¤È¤¢¤ëÀìÌç²È¤Ï¡¢Æ¬Éô¤Î³°½ý¤¬apoE4°äÅÁ»Ò¤ò»ý¤Ã¤¿¿Í¡¹¤Ë¤È¤Ã¤Æ¤Î¤ß´í¸±¤Ç¤¢¤ë¤È¿®¤¸¤Æ¤¤¤Þ¤¹¡£ A blow to the head may aggravate the toxic effect of mercury in at least two ways: it might stress the body and thereby weaken the body's ability to withstand the presence of mercury;he trauma may fracture fillings and increase the victim's exposure to mercury.
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Her inability to concentrate and make decisions set in after a 1978 car accident.The problem was severe.
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These symptoms persisted until 1992 when her dentist discovered that several teeth in the upper right side of her mouth with amalgams in them were cracked.
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June speculates that the blow to her head suffered during her auto accident allowed mercury from her fillings to gain access to her brain.
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¡¡¡¡¡¡¡¡¡¡¡þ¡¡¡¡¡¡¡¡¡¡¡¡¡¡¡þ¡¡¡¡¡¡¡¡¡¡¡¡¡¡¡þ Finally, smoking seems to play a protective role against AD.
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The reason for this may be that nicotine has the opposite effect on neurotransmitters that mercury has.
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Whereas mercury inhibits the uptake of, or otherwise reduces the effect of, dopamine, norepinephrine, serotonin and acetycholine, nicotine increases the levels of these neurotransmitters.
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This may explain why people with amalgams tend to smoke more than people without amalgams.
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