Scientists at Northwestern University report that neurofibrillary tau tangles must be present for the development of Alzheimer's disease, possibly providing a new target for future treatments.

Both the tangles and beta-amyloid plaques have been linked to the disease, but researchers previously were unable to find a mechanism linking the two types of lesions (see earlier Alzheimer's Week story).

Results of a study appearing in the Proceedings of the National Academy of Sciences, however, show the tau tangels actually enable the beta-amyloid plaques to induce cell degeneration that causes the disease.

"Our results underscore the importance of tau in the pathogenesis of this devastating disease and open a new chapter in deciphering the toxic pathways activated by beta-amyloid," said Dr. Adriana Ferreira, assistant professor of cell and molecular biology and Northwestern University Institute for Neuroscience researcher.

Pointing to their key role in the development of beta-amyloid-induced neurodegeneration, Ferreira said that while neurons with normal amounts of tau degenerated in the presence of amyloid beta, those neurons specially treated to be devoid of tau did not degenerate.

"These results provide direct evidence supporting a key role for tau in the mechanisms leading to amyloid beta-induced neurodegeneration in the central nervous system," the researchers concluded.

Other Sources: Northwestern University, Proceedings of the National Academy of Sciences