DIAN-TU trial fails to prevent dementia in genetic version of AZ.
Gina Kolata NYT article link
Excerpts:
" The participants were the best candidates that scientists could find: still healthy, but with a rare genetic mutation that guaranteed they would develop dementia."
"Few experts want to give up on the hypothesis that amyloid plaques in the brain are intimately involved in Alzheimer’s disease."
"The study was small, with only 194 participants: 52 taking a drug called gantenerumab, made by Roche, and an equal number trying solanezumab, made by Eli Lilly. Most of the subjects had no symptoms; a few were experiencing very mild early symptoms. About 40 family members served as a comparison group, and received no medication.
The volunteers carried gene mutations that cause an overproduction of amyloid, which accumulates in hard plaques in the brain. That is enough to always cause Alzheimer’s disease. The experimental drugs attacked amyloid, and scientists like Dr. Bateman had hoped they would prevent cognitive decline."
"The disease, they note, always progresses in the same way: Amyloid accumulates in the brain and then a tangled, spaghetti-like protein, tau, appears and neurons die.
“Amyloid and tau define the disease. Bingo,” said Dr. Ronald Petersen, director of the Mayo Clinic Alzheimer’s Disease Research Center. “To not attack amyloid doesn’t make sense.”
Dr Bateman was quoted:
"There are four drugs intended to ease the decline, but none to alter the course of Alzheimer’s disease. “We don’t have anything now to treat these people,” he said."
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