Abstract
Nicotine addiction is prevalent in individuals with schizophrenia. Nicotine activation of nicotinic receptors (nAChRs) is time- and dose-dependent, but gene expression analyses often rely on qualitative self- or family-reported measures of smoking. We sought lymphocyte surrogates for cerebral α7-nAChR activity and tested if receptor transcription correlated with concurrently measured serum biomarkers for smoking [cotinine, C-reactive protein (CRP)]. PCR surveys to detect lymphocytic α7-related isoforms identified CHRFAM7A as the only consistently amplifiable transcript. In 20 smoking-matched people (n = 10 schizophrenia, n = 10 controls), we found significantly lower CHRFAM7A in cotinine and self-reported smokers versus nonsmokers (p ≤ 0.001-0.03) and an inverse correlation of cotinine with CHRFAM7A (p ≤ 0.04) in regression models. CHRFAM7A was not associated with diagnosis or CRP in any bi- or multi-variate analysis. Smoking-related CRP elevations only occurred in cotinine-based comparisons (p ≤ 0.03), and not when smoking was self-reported. Including biochemical indicators of serum nicotine can help differentiate smoking- versus disease-associated changes in nAChR expression.
Original language | English (US) |
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Pages (from-to) | 213-220 |
Number of pages | 8 |
Journal | Journal of Neural Transmission |
Volume | 116 |
Issue number | 2 |
DOIs | |
State | Published - Feb 2009 |
Keywords
- Alpha7 nicotinic receptor
- Biomarker
- Inflammation
- Nicotinic acetylcholine receptor
- Peripheral blood monocytes
- Smoking
ASJC Scopus subject areas
- Neurology
- Clinical Neurology
- Psychiatry and Mental health
- Biological Psychiatry