Smoking cessation and Alzheimer's disease: facts, fallacies and promise.

Expert Review of Neurotherapeutics (Impact Factor: 2.83). 05/2010; 10(5):629-31. DOI: 10.1586/ern.10.34
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Available from: Janine K Cataldo, Jan 14, 2014
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    ABSTRACT: Neuronal nicotinic acetylcholine receptors (nAChRs) are a family of ligand-gated ion channels which are widely distributed in the human brain. Several lines of evidence suggest that two major subtypes (α4β2 and α7) of nAChRs play an important role in the pathophysiology of Alzheimer's disease (AD). Postmortem studies demonstrated alterations in the density of these subtypes of nAChRs in the brain of patients with AD. Currently, nAChRs are one of the most attractive therapeutic targets for AD. Therefore, several researchers have made an effort to develop novel radioligands that can be used to study quantitatively the distribution of these two subtypes in the human brain with positron emission tomography (PET) and single-photon emission computed tomography (SPECT). In this paper, we discuss the current topics on in vivo imaging of two subtypes of nAChRs in the brain of patients with AD.
    12/2010; 2010:548913. DOI:10.4061/2010/548913
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    ABSTRACT: Background: Cigarette smoking has been linked with both increased and decreased risk for Alz-heimer's disease (AD). This is relevant for the US military because the prevalence of smoking in the military is approximately 11% higher than in civilians. Methods: A systematic review of published studies on the association between smoking and increased risk for AD and preclinical and human literature on the relationships between smoking, nicotine exposure, and AD-related neuropathology was conducted. Original data from comparisons of smoking and never-smoking cognitively normal elders on in vivo amyloid imaging are also pre-sented. Results: Overall, literature indicates that former/active smoking is related to a significantly increased risk for AD. Cigarette smoke/smoking is associated with AD neuropathology in preclinical models and humans. Smoking-related cerebral oxidative stress is a potential mechanism promoting AD pa-thology and increased risk for AD. Conclusions: A reduction in the incidence of smoking will likely reduce the future prevalence of AD. Ó 2014 The Alzheimer's Association. All rights reserved. * This is an open access article under the CC BY-NC-ND license (http:// Publication of this article was supported by the United States Army Medical Research and Materiel Command. M.W.W. has served on the Scientific Advisory Boards for Pfizer, BOLT International, Neurotrope Bioscience, and Eli Lilly. He has provided consul-ting to Synarc,, and Genentech. He served on the Editorial Boards for Alzheimer's & Dementia and MRI. He received honoraria from Pfizer Inc, Tohoku University, and Danone Trading, BV. He received research support from Merck, Avid, the Veterans Administration (VA) and Department of Defense (DOD). The other authors have no conflict of interest to report.
    Alzheimer's and Dementia 06/2014; 10(3):S122-S145. DOI:10.1016/j.jalz.2014.04.009 · 17.47 Impact Factor
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    ABSTRACT: Chronic alcohol-use disorders (AUDs) have been shown to interact with normal age-related volume loss to exacerbate brain atrophy with increasing age. However, chronic cigarette smoking, a highly co-morbid condition in AUD and its influence on age-related brain atrophy have not been evaluated. We performed 1.5 T quantitative magnetic resonance imaging in non-smoking controls [non-smoking light drinking controls (nsCONs); n = 54], smoking light drinking controls (sCONs, n = 34), and one-week abstinent, treatment-seeking alcohol-dependent (ALC) non-smokers (nsALCs, n = 35) and smokers (sALCs, n = 43), to evaluate the independent and interactive effects of alcohol dependence and chronic smoking on regional cortical and subcortical brain volumes, emphasizing the brain reward/executive oversight system (BREOS). The nsCONs and sALCs showed greater age-related volume losses than the nsALCs in the dorsal prefrontal cortex (DPFC), total cortical BREOS, superior parietal lobule and putamen. The nsALCs and sALCs demonstrated smaller volumes than the nsCONs in most cortical region of interests (ROIs). The sCONs had smaller volumes than the nsCONs in the DPFC, insula, inferior parietal lobule, temporal pole/parahippocampal region and all global cortical measures. The nsALCs and sALCs had smaller volumes than the sCONs in the DPFC, superior temporal gyrus, inferior and superior parietal lobules, precuneus and all global cortical measures. Volume differences between the nsALCs and sALCs were observed only in the putamen. Alcohol consumption measures were not related to volumes in any ROI for ALC; smoking severity measures were related to corpus callosum volume in the sCONs and sALCs. The findings indicate that consideration of smoking status is necessary for a better understanding of the factors contributing to regional brain atrophy in AUD.
    Addiction Biology 09/2012; DOI:10.1111/j.1369-1600.2012.00492.x · 5.93 Impact Factor