Nicotine, neurodegeneration, and neuroprotection in neuropsychiatric disorders

Susan E. Maloney, Kuryn M. Kroutil, George T. Taylor

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review


This chapter reviews the relation of nicotine to brain function and dysfunction. The emphasis is on the influences of nicotine on neurodegeneration and neuroprotection of consequent psychopathology. Topics covered include data from animal models and human patients on behavioral consequences on disorders of memory, traumatic brain injury, mood disorders, and schizophrenia. For example, cigarette smoking is related to a reduced incidence and severity of the symptoms of Parkinson's disease. The neuroprotective mechanism of acute and chronic exposure appears to involve the genes that regulate nicotinic cholinergic receptors. Laboratory evidence suggests nicotine facilitates cognitive recovery and attenuates synaptic disruptions following brain injury. Nicotine may be an effective agent in modifying the progression of the cognitive correlates of schizophrenia. Indeed, the percentage of schizophrenia patients who choose to smoke is remarkably high. The same is found in bipolar mood disorders. However, bipolar patients who smoke experience a worse outcome than non-smoking patients. These data call into question the often-stated hypothesis that psychiatric populations self-medicate with nicotine. In conclusion, evidence is equivocal, but nicotine appears to be neuroprotective under certain pathological conditions. Therefore, nicotine analogues may be useful in the treatment of behavioral deficits of some neurodegenerative diseases, various types of neural injury, or certain psychiatric disorders.

Original languageEnglish
Title of host publicationNicotine Addiction
Subtitle of host publicationPrevention, Health Effects and Treatment Options
PublisherNova Science Publishers, Inc.
Number of pages36
ISBN (Print)9781620812907
StatePublished - Aug 1 2012


Dive into the research topics of 'Nicotine, neurodegeneration, and neuroprotection in neuropsychiatric disorders'. Together they form a unique fingerprint.

Cite this