Nicotine for Alzheimer's disease

López‐Arrieta, Jess; Sanz, Francisco

doi:10.1002/14651858.cd001749

Cited by 27 publications

(14 citation statements)

References 42 publications

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“…Epidemiological and pharmacological studies have established a relation between cigarette smoking and various diseases, such as coronary heart disease, peripheral vascular disease, cancer and others [1][2][3][4]. On the other hand, some epidemiological studies suggest that nicotine may have protective effects against degenerative processes such as Alzheimer's disease, Parkinson's disease, and Tourette's syndrome [5][6][7]. However, the mechanisms underlying these diverse associations are largely unknown.…”

Section: Introductionmentioning

confidence: 99%

Nicotine, Body Weight and Potential Implications in the Treatment of Obesity

Kane²,

Konu³

2003

CTMC

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Obesity is an epidemic problem in the U. S. and many other industrialized nations. Historically, the drugs used for the treatment of obesity generally targeted small molecule neurotransmitters. As research grows to decipher the underlying molecular mechanisms behind energy homeostasis, it is becoming evident that the modulating effects of neuropeptides also are critical in the regulation of appetite and metabolism. The search for drugs to modify these monoaminergic and peptidergic pathways may eventually prove successful in the treatment of obesity. While tobacco smoking has long been used as one strategy to maintain a lower body weight, especially in female smokers, its adverse associations with addiction and disease overshadow its potential use as an antiobesity agent. Potential pharmacological effects of nicotine could be better understood as the intricacies of the nicotinic acetylcholine receptor are revealed. The objective of this review is threefold: first is to provide an overview of the physiological effects of nicotine on body weight while focusing on the drugs that are available as antiobesity and smoking cessation agents. Second is to provide the present status of the nicotinic acetylcholine receptor as it relates to energy homeostasis and its potential as an effective treatment modality for obesity. Third is to present the current knowledge with respect to nicotine's effects on energy homeostatic and reward related pathways at the molecular level. A better understanding of the regulatory mechanisms underlying the pharmacological effects of nicotine on body weight will provide insights in identification of potential targets for the development of appropriate medicines in the treatment of obesity.

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Section: Introductionmentioning

confidence: 99%

Nicotine, Body Weight and Potential Implications in the Treatment of Obesity

Kane²,

Konu³

2003

CTMC

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“…Several theoretical and practical considerations have hindered the development of this therapeutic line: a) the side effects (cephalalgia, giddiness, anxiety, etc.) of nicotine overdose (Malizia et al, 1983; Singer y Janz, 1990; Benowitz, 1996); b) the low content of N‐receptors in AD (Aubert et al, 1992; Vidal, 1996; Terzano et al, 1998; Martín‐Ruiz, 1999; Guan et al, 2000; Perry et al, 2000; Wevers et al, 2000); c) the location of some kind of N‐receptors in cholinergic terminals, producing variable regulation of Ach release (Marchi and Raiteri, 1996; Lindstron, 1997); e) the consideration of nicotine as drug of abuse (i.e., tobacco) that exerts a number of neurodegenerative, behavioral and psychological effects (Baron, 1996; Perkins et al, 1996; Ulrich et al, 1997; Lena and Changeux, 1998; López‐Arrieta et al, 2000; Domino et al, 2000); f) the ubiquitous existence of N‐receptors, which could elicit a considerable number of side effects (Gotti et al, 1997; Lindstrom, 1997; Pontieri et al, 1998; Alburquerque et al, 2000; López‐Arrieta et al, 2000); and g) the desensitization of nicotine receptors induced by short‐term (Alburquerque et al, 2000) or long‐term use (Maelicke, 2000) of nicotine agonists, leading to tolerance and therefore limiting the duration of the efficacy of nicotine agonist treatment (Maelicke, 2000).…”

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confidence: 99%

Histochemical study of acute and chronic intraperitoneal nicotine effects on several glycolytic and Krebs cycle dehydrogenase activities in the frontoparietal cortex and subcortical nuclei of the rat brain

Turégano¹,

Martínez‐Rodríguez²,

Álvarez³

et al. 2001

J of Neuroscience Research

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The effects of nicotine on the activity of different dehydrogenases in frontoparietal regions and subcortical nuclei of the rat brain have been studied using histochemical methods. Nicotine sulphate was intraperitoneally administered in acute (4 mg/kg/day × 3 days) or chronic (ALZET osmotic pump providing 2 mg/kg/day × 15 days) doses. The enzymes analyzed were glyceraldehyde‐3‐phosphate, lactate, malate and succinate dehydrogenases (gly3PDH, LDH, MDH, and SDH, respectively). The results demonstrate that chronic as well as acute administration of nicotine produced strong increases in all these enzymatic activities in the superior layers (I, II and III) of the frontoparietal cortex (cingulate, motor and somatosensory regions); but high increases were not seen in the deeper layers of the cortex or in the subcortical nuclei (substantia nigra, caudate‐putamen, nucleus accumbens or nucleus basalis magnocellularis). These hyperactivities were produced in brain regions with normally low enzymatic activity (cortex), but not in those with great intensity (subcortical nuclei). The results are in rough agreement with previous reports on nicotine‐induced increases in glucose utilization, gly3PDH genic expression and neuronal hyperactivity in the brain cortex; but significant discrepancies between the cortical enzymatic maps and those obtained both in these studies and others on nicotine(N)‐receptor localization have been appreciated. The results support the hypothesis that nicotinic cholinergic drugs can have metabolic, long‐lasting stimulant effects on cortical neurons at specific points (probably layer III pyramidal cells and structures with α7‐N‐receptors) of the cortical circuits that could be of great interest in improving altered cognitive functions that are present in Alzheimer disease, as well as in other less severe mental disturbances. Mitochondrial hyperfunction should also be evaluated as a possible side‐effect (as an oxidative stress inductor) of these kinds of drugs. J. Neurosci. Res. 64:626–635, 2001. © 2001 Wiley‐Liss, Inc.

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“…Although systematic reviews have assessed nicotine as a treatment for Alzheimer's disease,1 Parkinson's disease23 or schizophrenia,15 trials have been small and the results inconclusive.…”

Section: Postulated Positive Effects Of Nicotinementioning

confidence: 99%

Nicotine and health

2014

DTB

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Nicotine, an alkaloid derived from the leaves of tobacco plants (Nicotiana tabacum and Nicotiana rustica) is the primary addictive agent in tobacco products.(1,2) There are different ways of administering the various products including smoking cigarettes, chewing tobacco, holding moist snuff in the mouth, inhaling dry snuff through the nose, inhaling smoke from a waterpipe and inhaling vapour from an electronic cigarette.(3-6) It can be difficult differentiating the effects of nicotine from the many other toxic substances these products also contain. Here we review the pharmacological effects of nicotine but we will not review the well-known harmful effects of cigarettes, where it is primarily the toxins and carcinogens in tobacco smoke rather than the nicotine that cause illness and death.(7) A future article will consider the use of electronic cigarettes.

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Nicotine for Alzheimer's disease

Cited by 27 publications

References 42 publications

Nicotine, Body Weight and Potential Implications in the Treatment of Obesity

Nicotine, Body Weight and Potential Implications in the Treatment of Obesity

Histochemical study of acute and chronic intraperitoneal nicotine effects on several glycolytic and Krebs cycle dehydrogenase activities in the frontoparietal cortex and subcortical nuclei of the rat brain

Nicotine and health

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