Schizophrenia, Monoamine Oxidase Activity, and Cigarette Smoking

Simpson, George M.; Shih, Jean C.; Chen, Kevin; Flowers, Calvin; Kumazawa, Takeshi; Spring, Bruce

doi:10.1016/s0893-133x(98)00119-5

Cited by 31 publications

(13 citation statements)

References 17 publications

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“…It also brings out the importance of reevaluating earlier reports that low platelet MAO B is a biological marker of vulnerability to psychiatric disorders in clinical populations where the rate of smoking is high, as has recently been done in the case of schizophrenia [81]. It also reinforces the need to look beyond nicotine as the only pharmacologically relevant substance in tobacco smoke to fully understand the behavioral and epidemiological characteristics of cigarette smoking.…”

Section: Tobacco Smoke Inhibits Maomentioning

confidence: 73%

Translational Neuroimaging: Positron Emission Tomography Studies of Monoamine Oxidase

et al. 2005

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Positron emission tomography (PET) using radiotracers with high molecular specificity is an important scientific tool in studies of monoamine oxidase (MAO), an important enzyme in the regulation of the neurotransmitters dopamine, norepinephrine, and serotonin as well as the dietary amine, tyramine. MAO occurs in two different subtypes, MAO A and MAO B, which have different substrate and inhibitor specificity and which are different gene products. The highly variable subtype distribution with different species makes human studies of special value. MAO A and B can be imaged in the human brain and certain peripheral organs using PET and carbon-11 (half-life 20.4 minutes) labeled mechanism-based irreversible inhibitors, clorgyline and L -deprenyl, respectively. In this article we introduce MAO and describe the development of these radiotracers and their translation from preclinical studies to the investigation of variables affecting MAO in the human brain and peripheral organs.

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Section: Tobacco Smoke Inhibits Maomentioning

confidence: 73%

Translational Neuroimaging: Positron Emission Tomography Studies of Monoamine Oxidase

et al. 2005

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“…Rich evidence shows a robust correlation between low MAO-B platelet activity and a spectrum of psychological traits related to behavioral disinhibition, such as sensation-seeking and novelty-seeking personality, extraversion, poor impulse control, and proclivity to engage in risky behaviors (Buchsbaum et al, 1976; Fowler et al , 1980; von Knorring et al, 1984; Reist et al , 1990; for a review, see Oreland and Hallman, 1995). While the discovery that smoking can reduce MAO-B activity (Simpson et al , 1999; Hauptmann and Shih, 2001) partially tempered this notion, in view of the high prevalence of this habit among sensation-seekers, further studies confirmed that the association between low MAO-B activity and novelty-seeking remain even after controlling for this environmental factor (Ruchkin et al , 2005). …”

Section: Phenotypical Outcomes Of Mao-b Deficitmentioning

confidence: 99%

Behavioral outcomes of monoamine oxidase deficiency: preclinical and clinical evidence

Bortolato

Shih

2011

International Review of Neurobiology

114

109

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Monoamine oxidase (MAO) isoenzymes A and B are mitochondrial-bound proteins, catalyzing the oxidative deamination of monoamine neurotransmitters as well as xenobiotic amines. Although they derive from a common ancestral progenitor gene, are located at X-chromosome and display 70% structural identity, their substrate preference, regional distribution, and physiological role are divergent. In fact, while MAO-A has high affinity for serotonin and norepinephrine, MAO-B primarily serves the catabolism of 2-phenylethylamine (PEA) and contributes to the degradation of other trace amines and dopamine. Convergent lines of preclinical and clinical evidence indicate that variations in MAO enzymatic activity—due to either genetic or environmental factors—can exert a profound influence on behavioral regulation and play a role in the pathophysiology of a large spectrum of mental and neurodegenerative disorders, ranging from antisocial personality disorder to Parkinson’s disease. Over the past few years, numerous advances have been made in our understanding of the phenotypical variations associated with genetic polymorphisms and mutations of the genes encoding for both isoenzymes. In particular, novel findings on the phenotypes of MAO-deficient mice are highlighting novel potential implications of both isoenzymes in a broad spectrum of mental disorders, ranging from autism and anxiety to impulse-control disorders and ADHD. These studies will lay the foundation for future research on the neurobiological and neurochemical bases of these pathological conditions, as well as the role of gene × environment interactions in the vulnerability to several mental disorders.

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“…Platelet MAO-B activity (only the B form is present in platelets) is a useful surrogate marker for the MAO-B activity in brain considering the biochemical and pharmacological resemblance of both isoenzymes (Donnelly and Murphy, 1977). Various groups have reported lower MAO-B activity in the blood platelets of tobacco smokers as compared to non-smokers (Berlin and Anthenelli, 2001;Norman et al, 1987;Oreland et al, 1981;Berlin et al, 1995b;Saccone et al, 1999;Simpson et al, 1999;Anthenelli et al, 1998). Using whole-body PET scans, Fowler et al (1996aFowler et al ( , 2003c first showed that smoking reduced the level of MAO-B in the brain and twelve peripheral organs (33 to 46% lower in smokers).…”

Section: Inhibition Of Mao In Tobacco Smokersmentioning

confidence: 99%

Contribution of monoamine oxidase (MAO) inhibition to tobacco and alcohol addiction

et al. 2006

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Schizophrenia, Monoamine Oxidase Activity, and Cigarette Smoking

Cited by 31 publications

References 17 publications

Translational Neuroimaging: Positron Emission Tomography Studies of Monoamine Oxidase

Translational Neuroimaging: Positron Emission Tomography Studies of Monoamine Oxidase

Behavioral outcomes of monoamine oxidase deficiency: preclinical and clinical evidence

Contribution of monoamine oxidase (MAO) inhibition to tobacco and alcohol addiction

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