New Alzheimer's therapy

A promising new Alzheimer's therapy appears to reduce the characteristic plaque build-up in the brains of Alzheimer's patients and to slow the rate of mental decline accompanying the disease.

In a study involving 165 Alzheimer's patients, half were given a placebo and the other half a monthly injection of an antibody called aducanumab.

Over the course of one year, the injected antibody caused the plaque to retreat and, crucially, slowed the cognitive degeneration that accompanies Alzheimer's disease. The antibodies work by selectively targeting a protein in the brain called amyloid-β (Aβ) - a neurotoxic plaque - and then binding with the protein and reducing the forms of it that are soluble and insoluble (like the fibers).

The new therapy was developed by researchers in the US and Switzerland and the results published in the science journal "Nature" on Wednesday (31.08.2016).

DW spoke to Alzheimer's expert Dr. Christian Haass of the German Center for Neurodegenerative Diseases (DZNE), who was not involved in the study, to put its importance into context.

DW: Are the results really "unprecedented," as the researchers say?

Dr. Christian Haass: In previous studies using similar approaches and similar antibodies, people were able to remove plaques - but it never resulted in a reduction of the memory loss. Or stabilization of the memory. So the big difference in this study is that the prevention, or reduction, of the amyloid plaque formation was strongly correlated with a stabilization of memory. And that's of course the major thing that you want. It's not enough to remove plaque. You need to stabilize memory.

So is this... it? Is this the cure for Alzheimer's?

It's a major, major, major advance in the field. It shows clearly that an anti-amyloid therapy can work and stabilize memory. As for a "breakthrough"... it may be too early. The study was small. But definitely, for the AD field [Alzheimer's/dementia], and for the patients, this is the first time that there's at least some beneficial effect on memory. That has never been found before, never ever.

Is there anything about this study you view critically?

There's a positive aspect to how they did it. You may have seen that many clinical trials doing it in a very similar way - with antibodies - failed. So they were capable of removing plaque, but there was no effect on memory. And many people basically said, "Well, that's the end of amyloid-based therapy, and immune therapy, because it just doesn't work. You remove plaques, but nothing happens to your memory." So what they did, what was clear from all the failed trials before, was that the disease's pathology begins decades before you see the first clinical symptoms, which is memory loss. So 10 to 20 years earlier, before you have your first memory deficits, you see amyloid plaque accumulation in these patients. And if you want to stop the disease, you have to treat the patients extremely early. So when they come in the clinic with strong memory loss - and that's usually happens with AD patients - it's too late. And what they did in the study is they used a very special imaging technology that can visualize amyloid plaque in the brain of living patients. And they looked for patients who had very, very, very mild cognitive impairment - so almost nothing. But they scanned them for the presence of amyloid plaques. And they only included people in the study who had already developed amyloid plaques. And this made the study extremely sensitive, because these patients were at a super early stage.

A major question for the last two-and-a-half decades in research for AD therapy was, "What is the cause of the disease?" And many people, including myself, always claimed it's amyloid production. Amyloid is basically the component that forms amyloid plaque. So if you were to stop amyloid production, you should stop the disease. And there's a lot of genetic evidence that this is indeed the case, also in humans. There's a lot of evidence in animal research that this is the case. But what was missing all the time was an amalyoid-based therapy that really stops memory decline. And this is the first time that there's proof of that. So for me, this is the end of this discussion. Amyloid indeed is the trigger of the disease.

Dr. Christian Haass is a professor of biochemistry