From the Scotsman

There is a row in Scotland over the availability of the prescription drug Memantine by the National Health Service, where it has been shown to delay admissions to eldercare facilities. An estimated 61,000 people in Scotland have been diagnosed with Alzheimer's or dementia....

In keeping with the global penomenon of memory loss, this article just appeared in Innovations-Report , a German web site devoted to scientific advance, reprinted from the Journal Neuron

Michael Addicott


Northwestern University researchers have prevented learning and memory deficits in a model of Alzheimer’s disease using a gene-targeting approach to block production of beta-amyloid, or "senile," plaques, one of the hallmarks of the disease.

Alzheimer’s disease is a neurodegenerative condition affecting over 15 million people worldwide that causes memory loss and, ultimately, dementia. Some research suggests that Alzheimer’s disease is caused by an increased amyloid burden in the brain -- the so-called amyloid cascade hypothesis.

Results of the Northwestern study, published in the January issue of the journal Neuron, provide compelling evidence for the therapeutic potential of inhibiting an enzyme, beta-secretase (BACE1), required for the production of beta-amyloid, to treat memory impairment in patients with Alzheimer’s disease.

The study also presents new evidence that beta-amyloid is directly responsible for causing the memory-robbing effects of Alzheimer’s disease, said Masuo Ohno, research assistant professor of physiology, Feinberg School of Medicine at Northwestern University. Ohno’s co-researchers on the project were John F. Disterhoft, professor of physiology, and Robert Vassar, associate professor of cell and molecular biology at the Feinberg School.