Researchers identify common type of dementia similar to Alzheimer’s

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By Linda Carroll

Scientists have been puzzled by patients with signs of dementia, but whose brains don’t show the aberrant proteins that are typical biomarkers of Alzheimer’s disease. Now researchers say they have an explanation: a newly defined neurodegenerative disease whose symptoms are similar to Alzheimer’s but is caused by a different misbehaving protein.

The disease, called LATE, seems to develop more slowly than Alzheimer’s and to appear later in life, when people are in their 80s and 90s, an international team of researchers reported Tuesday in the journal Brain. The brains of people who develop the disease don’t contain the protein amyloid beta, which causes plaques to develop between nerve cells, or tau, which grows tangles that clog the interiors of cells, eventually killing them.

“All over the world we saw very old people who had deterioration of their faculties and dementia, but no plaques and tangles,” said the report’s lead author, Dr. Peter Nelson, a professor of pathology at the Sanders-Brown Center on Aging at the University of Kentucky. “This explains a lot of that.”

LATE affects more than 1 million Americans, according to Nelson. “If you go to any nursing home, you’ll see evidence of it,” he said.

About 75 percent of people get Alzheimer’s disease, and some develop both Alzheimer’s and LATE, in combination, hastening the descent into dementia.

Knowing which protein is affecting the brains of seniors is significant since therapies being developed to treat Alzheimer’s disease target amyloid beta and tau. Medications designed to knock out those proteins won’t make a dent in a disease caused by the LATE protein, TDP-43.

That may explain the failures of some very promising Alzheimer’s drugs. The new report “won’t advance treatment today or tomorrow but it will help us understand why some of the treatments in the past failed,” said Dr. Richard Isaacson, director of the Alzheimer’s Prevention Clinic at NewYork-Presbyterian and Weill Cornell Medicine.

If 40 percent of the people in a clinical trial testing a drug that targets amyloid beta “didn’t even have amyloid in their brains, the study failed because it enrolled the wrong patients,” said Isaacson, who was not involved in the new report.