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Potential Therapeutic Benefits

The MIND Study is by far the largest and longest-running study of its kind, testing whether nicotine can improve memory loss.

Animal Study
Taken together, these results demonstrate that nicotine prevents memory deficits and synaptic impairment induced by Aβ oligomers. In addition, nicotine improves memory in young APP/PS1 transgenic mice before extensive amyloid deposition and senile plaque development, and also in old mice where senile plaques have already formed.
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- Citation: Inestrosa, N.C., Godoy, J.A., Vargas, J.Y. et al. Nicotine Prevents Synaptic Impairment Induced by Amyloid-β Oligomers Through α7-Nicotinic Acetylcholine Receptor Activation. Neuromol Med 15, 549–569 (2013). doi: 10.1007/s12017-013-8242-1
  - Acknowledgements: We thank Dr. Rodrigo Varas for his help with the electrophysiological studies of the α7-nAChR. This work was supported by a grant from FONDECYT No 120156 to N.C.I; predoctoral fellowships from CONICYT to G.G.F., M.S.A. F.G.S., J.A.R. and from Fundación Gran Mariscal de Ayacucho to J.Y.V. The Basal Center of Excellence in Science and Technology CARE was funded by CONICYT/PFB 12/2007.

Human and Animal Studies
Clinical trials and case series report anti-aggressive effects of nicotine. Here we argue that the nAChR system, the molecular basis for the global public health problem of tobacco smoking, may also be a key target for modulation of aggressive behaviors. Future research should aim to clarify which forms of aggression are most strongly affected by nAChR modulation, identify the nAChR subtypes, circuits, and neurobiological mechanisms of nicotine action, and determine whether more selective nAChR-active agents can replicate or improve the serenic effects of nicotine, especially with chronic dosing. Given the prevalence of aggressive behaviors across neuropsychiatric disorders affecting the very young to the very old, these studies have the potential to have a significant impact on public health.
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- Citation: Alan S. Lewis, Marina R. Picciotto, Regulation of aggressive behaviors by nicotinic acetylcholine receptors: Animal models, human genetics, and clinical studies, Neuropharmacology, Volume 167, 2020, 107929, ISSN 0028-3908, doi: 10.1016/j.neuropharm.2019.107929.
  - Acknowledgements: This work was supported by National Institutes of Health grants MH116339 (A.S.L.), MH077681 and DA14241 (M.R.P.).

Nicotine improves cognitive performance in clinical and preclinical studies.
Nicotine may also benefit depressive symptoms and depressive behavior.
Cognitive and mood benefits may be mediated by nicotinic effect on neural networks.
Nicotine’s effects on networks may reverse network changes seen in depression.
Improvement to mood and cognition may particularly benefit older depressed adults.
Both preclinical and clinical studies support that nicotine and other nAChR agonists can improve depressive behavior, mood, and cognitive performance. nAChR agonists also demonstrate neuropharmacologic effects that oppose the intrinsic network alterations reported in MDD. Through modulation of intrinsic functional networks, nAChR agonists may reduce depressive symptoms, enhance emotional regulation ability, and improve cognitive deficits common in LLD. For these reasons, we propose nAChR agonists as a potential novel treatment for the mood and cognitive symptoms of LLD.
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- Citation: Gandelman, J. A., Newhouse, P., & Taylor, W. D. (2018). Nicotine and networks: Potential for enhancement of mood and cognition in late-life depression. Neuroscience & Biobehavioral Reviews, 84, 289–298. doi:10.1016/j.neubiorev.2017.08.0
  - Acknowledgement: Supported by NIH grants K24 MH110598 and CTSA award UL1TR000445 from the National Center for Advancing Translational Sciences.

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