The idea that has made Alzheimer's research possible for more than three decades is about to be ended.
The hypothesis that Alzheimer's is caused by a sticky substance is being challenged by scientists. A study will give an experimental anti-amyloid drug to people as young as 18 who have genes that can cause Alzheimer's in their 30s or 40s.
Despite removing amyloid from the brains of patients in the early stages of Alzheimer's, several experimental drugs have failed to prevent declines in memory and thinking. The idea that amyloid is the cause of a cascade of events that lead to the death of brain cells has been eroded by those failures.
"If that doesn't work, nothing will work," says a professor of neurology.
By the end of the year, patients will be able to enroll in the DIAN-TU primary prevention trial.
Dr. Alois Alzheimer was the first to describe the disease that would bear his name.
Alzheimer had the chance to conduct an autopsy on a woman who died at the age of 50 after experiencing memory loss and other symptoms of dementia. He noticed that the woman's brain had an unusual disease of the cerebral cortex.
In the 1980s, scientists showed that the plaques were made of a substance that exists in many forms in the brain, from single free-floating molecule to large assembly that form the sticky plaques.
Drugs that target different forms of amyloid have been used in the treatment of Alzheimer's. That approach makes sense.
Thousands of studies show that this is enough to cause Alzheimer's.
As the list of drug failures has grown, doubts about the amyloid hypothesis have increased.
In a study of Alzheimer's patients who received the anti-amyloid drug gantenerumab, the researchers were unable to stop the disease.
The amyloid plaques in their brain had been reversed by it. There was no proof of a thinking-memory benefit.
It's too early to abandon the amyloid hypothesis according to many scientists.
The first two clinical trials of penicillin did not go well. People did not say that the antibiotic theory is a bad idea.
Recent studies have shown that anti-amyloid drugs can be effective in preventing cognitive decline.
Several brain changes associated with the death of brain cells were delayed by gantenerumab.
According to a statement from the drug's maker, lecanemab appears to slow down the loss of memory and thinking in people with Alzheimer's disease.
Many studies of anti-amyloid drugs failed because they were given to people with amyloid plaques. It may not be possible to stop the process that leads to the death of brain cells.
The prevention trial is going to start treatment earlier.
He predicts that it will work and that it will work well. Those people will never get Alzheimer's if we can prevent the plaques from taking off.
The prevention study is based on the idea that when amyloid builds up in the brain, there will be changes.
The death of brain cells involved in thinking and memory is one of the changes.
We're trying to prevent that from happening in the first place.
Treatment will start long before symptoms show up.
The person probably had amyloid in their brain for a long time.
The study will enroll 160 people from families with Alzheimer's disease. This form of dementia is caused by rare, inherited genes that cause Alzheimer's to develop in people in their 30's and 40's.
The earliest they can be admitted is 25 years from now. When we're going to start this trial, most of these families will be in their 20s.
The anti-amyloid drug gantenerumab will be used in this study.
Ensuring that amyloid plaques don't show up is the short term goal. The appearance of other markers of Alzheimer's effects on the brain will be looked at.
One of the markers is the presence of neurofibrillary tangles, a toxic version of aprotein calledtau that forms disorganized threads inside a neuron The internal tangles disrupt a cell's ability to move and maintain connections.
Brain atrophy is a decline in one or more brain areas caused by the loss of neuron and the connections between them.
"If we prevent amyloid pathology from developing and these other markers continue to develop and unfold, this would be one of the best ways to say, listen, amyloid is not what we should be targeting."
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