The disease seems to develop more slowly than Alzheimer’s and appears later in life, researchers report.
There are some similarities between the two proteins that cause Alzheimer’s and the one implicated in LATE. All three, in their normal states, perform necessary functions in the brain. In people who develop either disease the proteins start to fold in pathological ways, leading them to gunk up nerve cells and the spaces in between them.
“Proteins always get folded, but when they misfold, it causes a lot of problems,” Nelson said. “It produces toxic effects because the protein is impaired from its normal activities.”Without a biomarker for TDP-43, a brain autopsy after a patient dies is the only way doctors know for sure what was the underlying cause of dementia.
For now, researchers will have to depend on less reliable methods to distinguish between the two diseases. MRIs offer some hints because the pattern of nerve damage seen with LATE is slightly different from that seen in Alzheimer’s. The search for a biomarker becomes more urgent as people live longer, said Sandra Weintraub, a professor of psychiatry and behavioral sciences and a member of the Mesulam Center for Cognitive Neurology and Alzheimer’s Disease at Northwestern University. According to a 2018 report from the Centers for Disease Control and Prevention, by 2060, the number ofwill hit nearly 14 million, or about 3.3 percent of the projected population.
“This is a really important step carrying this field forward,” Weintraub said of the report. “People are living longer. And the more you prolong someone’s life, the more you increase their risk of getting this.”Linda Carroll is a regular health contributor to NBC News and Reuters Health. She is coauthor of"The Concussion Crisis: Anatomy of a Silent Epidemic" and"Out of the Clouds: The Unlikely Horseman and the Unwanted Colt Who Conquered the Sport of Kings.
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