Tobacco and ADHD: A Role of MAO-Inhibition in Nicotine Dependence and Alleviation of ADHD Symptoms

Abstract

Attention-deficit/hyperactivity disorder (ADHD) is a relatively commonly occurring neurodevelopmental disorder affecting approximately 5% of children and young people. The neurobiological mechanisms of ADHD are proposed to particularly center around increased dopamine receptor availability related to associated symptoms of reduced attention regulation and impulsivity. ADHD is also persistent across the lifespan and associated with a raft of impulsive and health-risk behaviors including substance abuse and smoking. Research highlighting the potentially significant levels of monoamine oxidase (MAO) inhibitory properties in tobacco smoke and e-cigarettes may provide a mechanism for increased tobacco smoke dependence among those with ADHD, in addition to the role of nicotine.AimThis scoping review aimed to establish evidence for the above neurobiological pathway between smoking and ADHD symptom-alleviation or “self-medication” with the inclusion of the mechanism of MAO-inhibitors indirect increasing dopamine in the brain.MethodologyScoping review methodologies were employed in this review selected to synthesize multiple sources of empirical research to identify current gaps in the knowledge base and identify key characteristics of research data related to a phenomenon. Databases searched included OVID MEDLINE(R), Embase, Cochrane, PsycINFO and SCOPUS limited to 2000 onward and empirically validated, peer-reviewed research.FindingsThere is support for the role of MAO-inhibition on greater reinforcement of smoking for individuals with ADHD through a greater impact on dopaminergic availability than nicotine; potentially moderating ADHD symptoms.ConclusionGreater support for a “self-medication” model of ADHD and smoking includes not only nicotine but also MAO-inhibitors as dopamine agonists contained in cigarettes and e-cigarettes.

Nicotinic Acetylcholine Receptors in Glial Cells as Molecular Target for Parkinson’s Disease

“…It is now evident that nAChRs not only play an important role in neuronal function and the addiction to nicotine [ 151 , 152 ] but may also serve as targets for therapeutic intervention in various neuropsychiatric/neurodegenerative disorders, including PD [ 25 , 153 , 154 ], depression [ 153 , 155 , 156 ], obsessive–compulsive disorder [ 157 , 158 ], ADHD [ 159 ], Tourette syndrome [ 160 , 161 , 162 ], mild cognitive impairment or Alzheimer’s disease [ 163 , 164 , 165 , 166 ], ischemia [ 167 ], catalepsy [ 168 ], schizophrenia [ 4 , 166 , 169 ], pain [ 147 , 170 ], energy balance [ 171 , 172 ], autoimmune disorders [ 173 ], and even sleep–wake cycle dysregulation [ 174 ]. These receptors are also expressed abundantly in a variety of immune cells, including B cells, T cells, macrophages, and microglia, and are believed to contribute to the anti-inflammatory effects of nicotine [ 175 , 176 , 177 , 178 ].…”

Nicotinic Acetylcholine Receptors in Glial Cells as Molecular Target for Parkinson’s Disease

“…It is now evident that nAChRs not only play an important role in neuronal function and addiction to nicotine [151,152], but may also serve as targets for therapeutic intervention in various neuropsychiatric/neurodegenerative disorders including PD [25,153,154], depression [153,155,156], obsessive-compulsive disorder [157,158] , ADHD [159], Tourette syndrome [160][161][162], mild cognitive impairment or Alzheimer's disease [163][164][165][166], ischemia [167], catalepsy [168], schizophrenia [4,166,169], pain [147,170], energy balance [171,172], autoimmune disorders [173], and even in sleepwake cycle dysregulation [174]. These receptors are also expressed abundantly in a variety of immune cells including B cells, T cells, macrophages, and microglia, and are believed to contribute to the antiinflammatory effects of nicotine [175][176][177][178].…”