An Alzheimer’s Treatment Fails: “We Have Nothing Now”

An Alzheimer's Treatment Fails: "We Have Nothing Now"

Studies show that Alzheimer’s disease can be stopped if treatment begins before symptoms are revealed. The participants were the best candidates that scientists could find: still healthy, but with rare genetic mutations, they confirmed they would develop dementia.

For five years, volunteers received monthly blood tests, brain scans, spinal cord and cognitive tests, as well as monthly infusions or injections of one of two experimental drugs.

Now, the verdict is on: drugs have done nothing to slow or stop cognitive decline in these subjects, dashing the hope of scientists.

Neurologist and principal investigator of the study at Washington University in St. Louis. Randall Batman says he was “shocked” when he first saw the information: “It was really crushing.”

The results are a profound disappointment, scientists said – but not a knockout punch. The drugs don’t work, but the problems can be fixed: perhaps the dose was too low, or their patients should have been given too young.

Very few experts want to abandon the hypothesis that amyloid plaques in the brain are closely involved in Alzheimer’s disease.

The data from this international study, known as DIAN-TU, are still being analyzed and will be presented at scientific conferences in Vienna on April 2nd and Amsterdam in July.

The test was sponsored by the University of Washington, St. Louis, a subsidiary of Eli Lilly and Roche – a subsidiary of the National Institutes of Health and Charities, including the Altihar Association.

The study was short, with only 194 participants: 52 took a drug called Gantenerumab made by Rant, and an equal number of Solenzumab were made by Eli Lilly. Most of the subjects had no symptoms; Some were experiencing very mild symptoms at the very beginning. About 40 family members served as a comparison group and did not receive any drugs.

Volunteers cause excessive production of amyloid as a result of gene alterations that result in strong brain damage. Always enough for Alzheimer’s disease. The experimental drugs attacked amyloid, and scientists like Dr. Batman hoped they would prevent cognitive decline.

Participants in DINAU-TU were generally younger than Alzheimer’s patients, and other brain abnormalities, such as mini-strokes, had not yet been detected. The success of this experiment, it was hoped, showed that Alzheimer’s could be overcome.

Eli Lilly’s chief scientific officer. “This was a courageous test run by patients with a deep unmet medical need,” said Daniel Skovronsky.

Now companies and academic researchers must face a worrying question: Is it time to emphasize the development of anti-amyloid drugs for Alzheimer’s disease?

Studies of anti-amyloid drugs are still underway in older people. Scientists are testing drugs in the same group as DIAN-TU: A large family of Colombians also carry gene mutations that lead to Alzheimer’s at first.

Until now, studies of anti-amyloid drugs have repeatedly failed. Companies have spent billions of dollars on drugs. Someone like Pfizer is completely out of the race.

Many researchers have stated that they are not yet ready to leave.

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.

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