In the latest online edition of the Proceedings of the National Academy of Sciences, the researchers report that chronic nicotine exposure increases neurofibrillary tangles -- the bundles of fibers that are one of the two neuropathological hallmarks of the disease, the other being clump-like plaques. Previous animal studies had suggested that nicotine reduces the number of these plaques; however, this possible benefit is outweighed by the increase in tangles.

The paper will appear also in the Feb. 22 print edition of PNAS.

Alzheimer's disease is a slow, progressive disease and the most common cause of dementia among the elderly in the United States, affecting 4.5-5 million adults -- 10 times more than those affected by Parkinson's disease. The disease is marked by the accumulation of two distinct brain lesions -- beta-amyloid plaques and neurofibrillary tangles -- which accumulate in specific brain regions critical to learning and memory.

"In earlier work, we showed that plaques can induce tangles," said Salvatore Oddo, graduate student in the School of Biological Sciences' Department of Neurobiology and Behavior, and the first author of the paper. "But that is only one way in which tangles can form. There are other pathways, independent of plaques, that can lead to the formation of tangles. One of these, our work shows, is nicotine. It increases tangles independent of plaques, and, therefore, should not be used as a treatment for Alzheimer's disease."

To determine whether nicotine has a preventative effect on both lesions of Alzheimer's disease, the researchers administered the drug in the drinking water of 20 mice that were genetically engineered to develop both the plaques and the tangles
'"/>

Contact: Iqbal Pittalwala
iqbal@uci.edu
949-824-3969
University of California - Irvine
8-Feb-2005