Persons suffering from schizophrenia, depression or anxiety disorders use tobacco more than the general population suggesting that this is a form of self-medication. Chronic stress exacerbates many psychiatric conditions leading to working memory deficits, depression and anxiety.
We found that oral Cotinine, the main metabolite of nicotine, at doses about ten times the one attained from tobacco smoking reduces depressive behavior, anxiety and ameliorates memory loss in rodent models of psychological stress and Alzheimer’s disease. These antidepressant and nootropic effects were associated with an increase in the number of synapses that are the site of communication between neurons and which mediates the learning and memory process as well as the brain plasticity required for recovery from traumatic events and depression.
Also, these beneficial effects were accompanied by biochemical changes in the brain that have been also observed with the use of other antidepressants. These changes included the increase in the expression of proteins such as the vascular endothelial factor VEGF which expression is also enhanced by fluoxetine (antidepressant) and stimulates the growth of new neurons in the adult brain (neurogenesis).
Since cotinine when tried in humans did not show significant side effects, our results suggest that cotinine may be a new antidepressant and memory enhancer useful to treat Alzheimer’s disease as well as other condition leading to working memory loss. Actually, my main goal is to demonstrate in clinical trials the effectiveness of cotinine for treating Alzheimer’s disease.
Due to the fact government funds have been very elusive, in spite of the publication of numerous manuscripts with our results in prestigious peer-reviewed journals, we are planning a fundraising effort to support a pilot clinical study.
photo credit: The Department of Veteran Affairs http://www.baypines.va.gov