The disease, called LATE, often reflects the symptoms of Alzheimer's disease, although it affects the brain differently and develops more slowly than Alzheimer's. Doctors say the two are often found together, and in these cases, there could be a steeper cognitive decline than both.
In preparing their report, the international team of authors hopes to stimulate research – and perhaps one day, treatments – for a disease that tends to affect people over 80 and "has a growing but unrecognized impact on public health", it says in the newspaper.
"We are really revising the concept of dementia," said lead author Dr. Peter Nelson, Director of Neuropathology at the University of Kentucky Medical Center.
"There will not be a single disease that causes all forms of dementia," said Sandra Weintraub, Professor of Psychiatry, Behavioral Science and Neurology at the School of Medicine at Northwestern University Feinberg. She was not involved in the new work.
Weintraub said the researchers are aware of the "heterogeneity of dementia," but figuring out why each guy looks so different was a challenge. Why do some people lose memory first while others lose their language or show personality changes? Why do some people develop dementia earlier, while others develop it later?
Experts say that this heterogeneity has complicated dementia research, including Alzheimer's disease, because it was not always clear what the cause was ̵
What is it?
The acronym LATE stands for limbic-predominant age-related TDP-43 encephalopathy. The full name refers to the region in the brain most likely to be affected, as well as the protein in the center.
"These age-related dementias are often associated with proteinaceous Glop," Nelson said. "But different proteins can contribute to the glop."
Alzheimer's find a set of glops. At Lewy Body Dementia another blow.
And in LATE, the Glop is a protein called TDP-43. Doctors are not sure why the protein is found in a modified, misfolded form in a disease like LATE.
"This is an area that will be very large in the future, which individual vulnerabilities will cause the proteins to reach certain regions of the brain?" She said. "It's not just what the protein abnormality is, but where it is."
More than a decade ago, doctors first linked the TDP protein to amyotrophic lateral sclerosis, also known as ALS or Lou Gehrig's disease. It was also associated with another type of dementia called frontotemporal lobar degeneration.
LATE "is a disease 100 times more common than the two, and no one knows about it," says Nelson.
The New Paper Estimates Based on autopsy studies, 20 to 50% of people have over 80 brain changes related to LATE. And this prevalence increases with age.
Experts say nailing these numbers – and finding better ways to detect and explore the disease – is what they hope for, from consensus statements like the new paper that gives scientists an impression, according to Nelson a common language to discuss it.
"People have found different parts of the elephant in their own bailiwicks," he said. "But here everyone meets for the first time and says," That's the whole elephant. "
What this could mean for Alzheimer's
The new guidelines could also have implications for Alzheimer's research. First, experts say that some high-profile drug trials have suffered as a result of some patients not identifying LATE and therefore not responding to the treatment.
In fact, Nelson's colleagues recently saw this first hand: A deceased patient who participated in an Alzheimer drug study but still suffered from dementia.
"The clinical trial was thus a failure of Alzheimer's disease," Nelson said It turned out that he had no Alzheimer's disease. He had LATE. "
"I & # 39; I'm sure it matters, but not as much as you might think at first, "said Silverberg, who co-chaired the working group that led to the new paper.
Progress on testing They had already shown that some patients lacked "the tell-tale signs of Alzheimer's disease" in these studies, yet unrecognized pathologies that people could have, "she added.
"We could go back and examine all people who have failed their Alzheimer's disease therapies," Nelson said. "But what we really need to do is move forward and try to get these people out of clinical Alzheimer's trials – and bring them into their own clinical trials instead."
Silverberg describes the new paper as a "roadmap" for research that could change as we learn more about the disease. And researchers can not do this without a large, diverse group of patients, she added.
"It will probably take years for research participants to help understand all this," she said.