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The disease, called LATE, can often reflect the symptoms of Alzheimer's disease, although it affects the brain differently and develops more slowly than Alzheimer's disease. Doctors say that both are frequently found together and that, in these cases, they can result in greater cognitive decline than either.
In developing its report, the international team of authors hopes to stimulate research – and perhaps someday treatments – against a disease that usually affects people over 80 and "has a growing but little-known impact. on public health, "according to the paper.
"We are in the process of revising the concept of what is dementia," said Dr. Peter Nelson, senior author, director of neuropathology at the University of Kentucky Medical Center.
"No disease will cause all forms of dementia," said Sandra Weintraub, a professor of psychiatry, behavioral science and neurology at Feinberg School of Medicine at Northwestern University. She was not involved in the new newspaper.
Weintraub said the researchers were well aware of "the heterogeneity of dementia", but that it was difficult to determine precisely why each type can be so different. Why do some people lose memory first, while others lose language or have personality changes? Why do some people develop dementia earlier in life, while others develop it later?
Experts say that this heterogeneity has complicated research on dementia, including Alzheimer's disease, because the root cause of the disease was not always clear – and therefore, if doctors treated the problems properly .
What is it?
The acronym LATE stands for predominantly "age-related TDP-43 encephalopathy". The full name refers to the area of the brain most likely to be affected, as well as to the protein at the center of everything.
"These age-related dementia diseases are often badociated with a protein glop," Nelson said. "But different proteins can contribute to the glop."
In Alzheimer's, you will find a set of gloves. In Lewy body dementia, another glop.
And in the end, the glop is a protein called TDP-43. Doctors do not know why the protein is in a modified form and misfolded in a disease such as LATE.
"This is an area that will be really huge in the future – what are the individual vulnerabilities that cause proteins to go to certain areas of the brain?" she says. "It's not just what the protein abnormality is, but where it is."
More than a decade ago, doctors first linked TDP protein to amyotrophic lateral sclerosis, also known as ALS or Lou Gehrig's disease. She was also linked to another type of dementia, called frontotemporal lobar degeneration.
LATE "is a disease that is 100 times more common than these, and no one knows it," Nelson said.
The new paper estimates, based on autopsy studies, that between 20 and 50% of people over 80 will have brain changes badociated with LATE. And this prevalence increases with age.
Experts say that identifying these numbers – as well as finding better ways to detect and study the disease – is what they hope to come from consensus statements such as the new document, which gives scientists a common language for discuss it, according to Nelson.
"People have, in their own separate crates, found different parts of the elephant," he said. "But it's the first place where everyone meets and says:" It's the whole elephant "."
What could it mean for Alzheimer's disease?
The new guidelines could also have an impact on Alzheimer's research. On the one hand, experts say that some clinical trials of high-profile medications may have suffered because some patients have unidentified LATE – and therefore do not respond to treatment.
In fact, Nelson's colleagues have recently witnessed this: a patient, now deceased, who was part of a clinical trial for the treatment of Alzheimer's disease, but still developed dementia.
"So, the clinical trial was a failure for Alzheimer's disease," said Nelson, "but it turned out that he was not suffering from the Alzheimer's disease.He had a TOTAL DISEASE ".
"I'm sure it plays a role, but perhaps not as much as you might think at first," said Silverberg, who co-chaired the working group that led to the new document.
Advances in the tests had already shown that some patients in these trials had "no telltale signs of Alzheimer's disease," she said.
In some cases, perhaps it was late – "and it is certainly possible that there are other pathologies that people might have yet unknown," she added.
"We could go back and track down all the people who had failed their treatments for Alzheimer's disease," Nelson said. "But what we really need to do is go ahead and try to get these people out of Alzheimer's clinical trials – and get them to participate in their own clinical trials."
Silverberg describes the new document as a "road map" for research that may change as we discover more about the disease. And researchers can not do it without a large and diverse group of patients, she added.
"It will probably take years and research participants to help us understand all of this," she said.
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