Editorial: Smoking cessation and Alzheimer's disease: Facts, fallacies and promise

Expert Review of Neurotherapeutics (Impact Factor: 2.78). 05/2010; 10(5):629-31. DOI: 10.1586/ern.10.34
Source: PubMed
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Available from: Janine K Cataldo, Jan 14, 2014
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    • "Additionally, the rate of regional atrophy demonstrated by smokers may have been diminished by a survivor effect [40], given the age range of participants in this study. This study has limitations that may affect the generalizability of the findings. "
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    ABSTRACT: Little is known about the effects of cigarette smoking on longitudinal brain morphological changes in the elderly. This study investigated the effects of a history of cigarette smoking on changes in regional brain volumes over 2 years in healthy, cognitively intact elderly individuals. We predicted that individuals with a history of cigarette smoking, compared with never smokers, demonstrate greater rate of atrophy over 2 years in regions that manifest morphological abnormalities in the early stages of Alzheimer's disease (AD), as well as in the extended brain reward/executive oversight system (BREOS), which is implicated in the development and maintenance of substance use disorders. Participants were healthy, cognitively normal elderly control subjects (75.9 ± 4.8 years of age) with any lifetime history of cigarette smoking (n = 68) or no history of smoking (n = 118). Data were obtained through the Alzheimer Disease Neuroimaging Initiative from 2005 to 2010. Participants completed four magnetic resonance scans over 2 years. A standardized protocol using high-resolution three-dimensional T1-weighted sequences at 1.5 T was used for structural imaging and regional brain volumetric analyses. Smokers demonstrated a significantly greater atrophy rate over 2 years than nonsmokers in multiple brain regions associated with the early stages of AD, as well as in the BREOS system. Groups did not differ on the rate of global cortical atrophy. A history of cigarette smoking in this healthy elderly cohort was associated with decreased structural integrity of multiple brain regions, which manifested as a greater rate of atrophy over 2 years in regions specifically affected by incipient AD as well as chronic substance abuse.
    Alzheimer's & dementia: the journal of the Alzheimer's Association 11/2012; 8(6):513-9. DOI:10.1016/j.jalz.2011.10.006 · 12.41 Impact Factor
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    • "Thus, in elderly individuals, chronic smoking appears to be associated with abnormalities in regions that also exhibit morphological abnormalities in the incipient stages of Alzheimer's disease (AD) (Krueger et al. 2010). Correspondingly , a history of chronic cigarette smoking, particularly heavy smoking (>one pack/day) during middle age, is strongly linked to significantly increased risk for development of AD (Cataldo & Glantz 2010; Rusanen et al. 2010). However, since chronic cigarette smoking was not considered in previous MR studies reporting greater age-related atrophy reported in AUD, despite its high co-morbidity with AUD, it is unknown if smoking influenced the level of atrophy observed. "
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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; 19(1). DOI:10.1111/j.1369-1600.2012.00492.x · 5.36 Impact Factor
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    • "Additional research that relates measures of brain neurobiological function/integrity to neurocognition is needed to better understand the mechanisms contributing to the poorer performance across multiple domains demonstrated by smokers. Irrespective of the potential mechanism(s) leading to the observed group differences, a history of chronic smoking during midlife is associated with greater cognitive decline in those ≥64 years of age (Deary et al., 2003; Starr et al., 2006; Whalley et al., 2005) as well as strongly linked to increased risk for Alzheimer disease (Anstey et al., 2007; Cataldo and Glantz, 2010; Rusanen et al., 2011). This information combined with the substantial mortality and morbidity associated with chronic smoking stresses the need for development of more efficacious behavioral and pharmacological treatments to facilitate sustained smoking cessation as well as greater emphasis on smoking prevention programs for adolescents and young adults. "
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    ABSTRACT: The majority of studies investigating the neurocognitive consequences of chronic smoking have been conducted with adults 60 years and older. Therefore, the scope of neurocognitive dysfunction associated with chronic cigarette smoking in middle age (i.e., 30-60 age range) has not been fully delineated. Twenty-seven (44±9 years of age; 4 females) non-smoking and 30 smoking (49±8 years of age; 4 females) participants completed a comprehensive neurocognitive battery and measures of fine motor dexterity and postural stability. All participants were free of biomedical or psychiatric conditions that may have influenced neurocognitive and motor function. Smokers performed significantly worse than non-smokers on the following domains: auditory-verbal and visuospatial learning, visuospatial memory, cognitive efficiency, executive skills, general intelligence, processing speed, fine motor dexterity and postural stability. The differences between smokers and non-smokers evidenced moderate to strong effect sizes and were not mediated by age, education, vocational level, estimated verbal intelligence or alcohol consumption. In smokers, a greater number of lifetime years of smoking was related to poorer performance on measures of cognitive efficiency, processing speed and visuospatial skills. Results from this middle-aged cohort replicated previous research and provides novel findings indicating that chronic smoking was associated with inferior performance on measures of general intelligence, visuospatial learning and memory and fine motor dexterity. Research that relates measures of neurobiological function/integrity to neurocognition is needed to better understand the mechanisms contributing to the poorer performance across multiple domains demonstrated by smokers.
    Drug and alcohol dependence 10/2011; 122(1-2):105-11. DOI:10.1016/j.drugalcdep.2011.09.019 · 3.42 Impact Factor
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