The final excuse for smoking - that it might reduce the risk of developing Alzheimer’s disease - has just been stubbed out, findings from an animal study suggest.

Past animal and human studies have indicated that nicotine exposure inhibits the formation of amyloid plaque, a key feature of Alzheimer’s disease. However, the new study shows that chronic nicotine use appears to worsen the effects of a brain protein called tau, which is responsible for the fibrous tangles that are the other hallmark of the disease.

So, at best, the effects of nicotine are probably canceled out, according to the researchers.

Dr. Frank M. LaFerla, from the University of California at Irvine, and colleagues administered nicotine to a genetically engineered strain of mice that develops Alzheimer’s disease.

Nicotine treatment produced an increase in nicotine receptors in the animals’ brains that correlated with a dramatic rise in the aggregation and activity of the tau protein. This indicates that the disease-causing effects of tau were worsened, the team reports in the Proceedings of the National Academy of Sciences.

Moreover, in these experiments, chronic nicotine administration had no effect on levels of soluble amyloid, the researchers point out.

The results emphasize the importance of assessing nicotine’s affects on all aspects of the disease, they write. “Our findings suggest that the use of nicotine as a potential therapy for Alzheimer’s disease should be reevaluated.”

SOURCE: Proceedings of the National Academy of Sciences, early edition February 7, 2005.