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Tobacco Compound Prevents Memory Loss in Alzheimer’s Mice

New research suggests that a compound derived from tobacco may prove useful in the fight against Alzheimer’s disease. Valentina Echeverria, a scientist at Bay Pines VA Healthcare System and an assistant professor of Molecular Medicine at USF Health, and colleagues studied the effects of cotinine, the major byproduct of nicotine metabolism, in a mouse model of Alzheimer’s disease. Unlike nicotine, cotinine is non-toxic. It is also longer-lasting than nicotine. Furthermore, its safety has already been demonstrated in human trials designed to evaluate its ability to relieve tobacco withdrawal symptoms. Results showed that mice treated with cotinine showed a 26% reduction in deposits of amyloid plaques, a characteristic of Alzheimer’s disease, and also prevented the accumulation of amyloid peptide oligomers. Furthermore, cotinine stimulated the signaling factor Akt, which promotes the survival of neurons and enhances attention and memory. Long-term administration revealed that cotinine appeared to wholly prevent spatial memory impairment in the animals. “We found a compound that protects neurons, prevents the progression of Alzheimer’s disease pathology, enhances memory and has been shown to be safe,” said Professor Echeverria. “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.”

Valentina Echeverria, Ross Zeitlin, Sarah Burgess, Sagar Patel, Arghya Barman, Garima Thakur, et al. Cotinine reduces amyloid-β aggregation and improves memory in Alzheimer's disease mice. J Alzheimers Dis. 2011 Feb 14. [Epub ahead of print]. DOI: 10.3233/JAD-2011-102136

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