Safe Tobacco Smoke Compound Protects Against Alzheimer's Disease

Results of a recent study suggest that cotinine, the major metabolic product of nicotine, may be an excellent therapeutic candidate for the treatment of Alzheimer's disease.

Cotinine, which is found in high concentrations in the blood and urine of smokers, does not have the negative cardiovascular and addictive properties as nicotine. As some data has indicated that smokers have lower incidence of Alzheimer's disease, investigators at the University of South Florida (Tampa, FL, USA) examined the effect of cotinine on the brains of mice that had been genetically engineered to develop a disease that closely mimics Alzheimer's disease.

They reported in the April 2011 online edition of the Journal of Alzheimer's Disease that cotinine reduced amyloid beta plaque deposition, improved working and reference memories, and inhibited amyloid beta oligomerization in the brains of transgenic 6799 AD (Alzheimer's disease) mice. Overall, there was a 26% reduction in deposits of amyloid plaques in the brains of the treated animals. In vitro studies further confirmed the inhibitory effect of cotinine on amyloid beta aggregation.

Cotinine stimulated Akt signaling, including the inhibition of glycogen synthase kinase 3-beta (GSK3-beta), which promotes neuronal survival and the synaptic plasticity processes underlying learning and memory in the hippocampus and cortex of wild type and AD mice.

"We found a compound that protects neurons, prevents the progression of Alzheimer's disease pathology, enhances memory, and has been shown to be safe," first author Dr. Valentina Echeverria assistant professor of molecular medicine at the University of South Florida. "It looks like cotinine acts on several aspects of Alzheimer's pathology in the mouse model. That, combined with the drug's good safety profile in humans, makes it a very attractive potential therapy for Alzheimer's disease."

Related Links:
University of South Florida