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Smoking in Bipolar Disorder: Contribution of Sensory and Cognitive Brain Functions and Genomics

Institution: University of California, Irvine
Investigator(s): Julie Patterson,
Award Cycle: 2019 (Cycle 29) Grant #: T29IP0601 Award: $498,582
Subject Area: Neuroscience of Nicotine Addiction and Treatment
Award Type: High Impact Pilot Award

Initial Award Abstract
Smoking rates are two to three times higher in those with bipolar disorder (BPD) compared to the general population, making them susceptible to the associated adverse health effects as well as mortality at an earlier age. Smoking also has been associated with worse illness course and outcome. Identification of biomarkers contributes to our understanding of nicotine addiction and can lead to advancing smoking cessation efforts in high risk populations such as BPD. Unfortunately nicotine can sometimes improve sensory and cognitive processes in individuals with psychiatric illness, underscoring the need to find smoking cessation treatments. Sensory gating, a trait measure of sensory processing and brain inhibitory function, is impaired in BPD and is an established biomarker confirmed by a number of studies. In SZ, smoking reverses the gating impairment and ameliorates some of the sensory and cognitive deficits. The potential for smoking to mediate these same measures in BPD has not been studied and may lead to biomarkers to guide understanding of nicotine addiction in this high-risk group. Genetic variations in nicotine and neurotransmitter associated genes have been separately associated with SZ, nicotine dependence, cognition and sensory gating but few studies have examined these interactions in BPD. Certain nicotinic acetylcholine receptor genes have been implicated in the etiology of BPD and the modulation of P50 sensory gating. Similarly cognitive tasks such as attention and memory can improve with nicotine. These relationships suggest that a combination of these measures, including the nicotinic cholinergic subunit genes, P50 sensory gating and cognition can provide the more accurate and comprehensive view of the pathology of smoking that is required before effective treatments can be designed. Toward this goal, we propose to investigate this in groups of smoking and non-smoking BPD patients with and without psychosis. Using this combinatorial approach the proposed study will provide information about the neuroscience of nicotine addiction in BPD and identify pathways or gene targets for novel smoking cessation treatments.