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TECHNOLOGY, DISCOVERY & INNOVATION. UPDATED ABOUT A MINUTE AGO.
You are here: Home / Health / Hopes for Alzheimer's Drug Dashed
Failed Study, Dimmed Hopes in Hunt for Alzheimer's Treatment
Failed Study, Dimmed Hopes in Hunt for Alzheimer's Treatment
By Tom Murphy Like this on Facebook Tweet this Link thison Linkedin Link this on Google Plus
PUBLISHED:
NOVEMBER
23
2016

A treatment for Alzheimer's failed to slow mental decline in a widely anticipated study, ending hope that researchers at Eli Lilly had finally found a drug that does more to help those suffering from the fatal, mind-robbing disease.

The pharmaceutical company's shares plunged Wednesday before markets opened.

The drug, solanezumab, missed the study's main goal when patients taking it did not experience a statistically significant slowing of cognitive decline -- which involves a person's ability to remember things -- compared to those taking a placebo or fake drug.

Solanezumab had already failed in two previous large studies of people with mild-to-moderate forms of the disease, but combined results announced in 2012 suggested that the drug might slow decline for those with the mildest symptoms. Lilly initiated another study with hopes of helping those patients.

Alzheimer's is a degenerative, fatal disease that impairs memory and thought. It is characterized by the buildup in the brain of a protein called amyloid beta that clumps together to form sticky plaques between nerve cells.

With more than 5 million people in the United States afflicted, it is the most common form of dementia. It is the sixth-leading cause of death in the U.S. and the only one without a way to prevent, cure or even slow its progression, according to the Alzheimer's Association.

Solanezumab (sol-ah-NAYZ-uh-mab) is delivered intravenously and binds to the amyloid protein to clear it from the brain before it clumps together forming plaques.

Some researchers think the proteins trigger Alzheimer's before they form the plaques, but they aren't certain yet whether those proteins or the plaques are a cause of the disease, or if they're just a symptom. Other companies are testing drugs in an attempt to remove the protein.

Alzheimer's experts had modest expectations for Lilly's latest study, in part because a statistically significant result -- which means a change is likely not due to random chance -- doesn't necessarily deliver a dramatic improvement in how patients live with the disease.

Keeping a patient at the same cognitive level for 18 months would be considered a "big win," Maria Carrillo, chief science officer for the Alzheimer's Association, said before results were announced Wednesday.

A positive result could have led to a better option compared to what is out there now. Current Alzheimer's treatments like Aricept and Namenda temporarily ease symptoms such as memory loss, confusion and agitation. They don't slow, stop or reverse the mental decline that occurs when the brain's nerve cells stop functioning normally.

Alzheimer's patients typically live an average of eight years after their symptoms become noticeable, during which the disease gradually erodes their memory and ability to think or perform simple tasks.

At least 18 other drugs are in late-stage testing, including several similar to solanezumab.

The failure of solanezumab doesn't necessarily doom other drugs that take the same approach, said Dr. Ronald Petersen, director of the Mayo Clinic Alzheimer's Disease Research Center. Petersen noted earlier this month that other drugs target amyloid beta proteins in different ways.

Even so, shares of other drugmakers developing Alzheimer's treatments, like Axovant Sciences Ltd. and Biogen Inc., dove in early trading Wednesday.

Shares of Eli Lilly and Co., based in Indianapolis, tumbled 13 percent, or $9.99, to $66 in premarket trading. Lilly said the study result will lead to a fourth-quarter charge of about $150 million before taxes.

© 2017 Associated Press under contract with NewsEdge/Acquire Media. All rights reserved.
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James E Tripp:
Posted: 2016-11-30 @ 3:01pm PT
June 27, 2016: Cannabinoids remove plaque-forming Alzheimer’s proteins from brain cells. Preliminary lab studies at the Salk Institute find THC reduces beta amyloid proteins in human neurons.

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