IT MAY eventually be possible to restore some of the lost cognitive function and learning ability of people with Alzheimer鈥檚 disease.
Michael Shelanski of Columbia University in New York and his colleagues knew that an enzyme called ubiquitin C-terminal hydrolase L1 (Uch-L1) is essential for ridding brain cells of unwanted proteins, and that the beta-amyloid protein that forms plaques in the brains of Alzheimer鈥檚 patients somehow stops production of this enzyme.
When they injected extra Uch-L1 into the brains of mice with the mouse equivalent of Alzheimer鈥檚 disease, the animals鈥� learning ability improved markedly. There was no change in the amount of beta-amyloid protein in their brains, however, which suggests that a defect in the degradation of proteins other than beta-amyloid may play an important role in the disease.
Advertisement
Most existing treatments and vaccines for Alzheimer鈥檚 aim to destroy the beta-amyloid plaques, or stop any more forming. 鈥淭he main message of our work is that even in the presence of the beta-amyloid, there are ways to improve brain function,鈥� says Shelanski.
