Silent brain changes precede Alzheimer’s

WASHINGTON – Alzheimer’s quietly destroys the brain long before symptoms appear, and now scientists have new clues about the domino-like sequence of these changes; a potential window for intervention someday.

A large study in China tracked middle-aged and older adults for 20 years using regular brain scans, spine exams and other tests.

Compared with those who remained cognitively healthy, people who eventually developed the mind-stealing disease had higher levels of Alzheimer’s-related proteins in their spinal fluid 18 years before diagnosis, researchers reported Wednesday. Then every few years, the study detected another so-called biomarker of brewing trouble.

Scientists don’t know exactly how Alzheimer’s occurs. One of the early symptoms is a sticky protein called beta-amyloid, which over time turns into plaques that clog the brain. Amyloid alone is not enough to damage memory; The brains of many healthy people contain a lot of plaque. An abnormal tau protein that forms neuron-killer tangles is one of several accomplices.

New research published in the New England Journal of Medicine provides a timeline of how these abnormalities accumulate.

Alzheimer’s expert Dr. from Columbia University, who was not involved in the research. Richard Mayeux said the importance of the study “should not be exaggerated”.

“Knowing the timing of these physiological events is critical” to test new ways to treat and perhaps ultimately prevent Alzheimer’s, he wrote in an accompanying editorial.

The findings have no practical significance yet.

More than 6 million Americans and millions more worldwide have Alzheimer’s, the most common form of dementia. There is no cure. But last year, a drug called Leqembi became the first to be approved with clear evidence that it could slow the worsening of early Alzheimer’s disease, even by a few months.

It works by clearing some of this sticky amyloid protein. The approach is also being tested to see whether it is possible to delay the onset of Alzheimer’s if high-risk people are treated before symptoms appear. Other drugs targeting tau are also being developed.

Tracking silent brain changes is crucial for this type of research. Scientists already knew that in rare, inherited forms of Alzheimer’s that affect young people, a toxic form of amyloid begins to accumulate about two decades before symptoms appear, and at some point tau comes into play.

The new findings show the order in which such biomarker changes occur in the more common senile Alzheimer’s disease.

Researchers at the Beijing Innovation Center for Neurological Disorders compared 648 people who were eventually diagnosed with Alzheimer’s and the same number of people who remained healthy. The first finding of amyloid in future Alzheimer’s patients was either 18 years or 14 years before diagnosis, depending on the test used.

Differences in tau were later detected, followed by a sign of trouble with how neurons communicate. The study found that after a few years, differences in brain shrinkage and cognitive test scores between the two groups became apparent.

“The more we know about viable Alzheimer’s treatment targets and when to address them, the better and faster we will be able to develop new treatments and preventive measures,” said Claire Sexton, senior director of scientific programs at the Alzheimer’s Association. Blood tests are coming soon that promise to help by making it easier to track amyloid and tau, she noted.